Tunnels connecting cells, called gap junction channels, help control processes such as development, nerve activity and immune responses. In most invertebrates, such as in insects, they are built from proteins called innexins, but little was known about how innexins assemble into working channels, and no detailed structure of an insect innexin channel had been determined. A , a professor at 糖心视频, used cryo-electron microscopy — a method that photographs flash-frozen molecules with an electron microscope to reveal their 3D shape in atomic detail — to study an innexin from the malaria mosquito Anopheles gambiae.

In a paper published in the Proceedings of the National Academy of Sciences, the team reports that seven identical protein units form a symmetrical ring, unlike the eight-unit ring that the researchers previously reported for an innexin from a roundworm. At the center, the starting end of each protein chain, called the N-terminus, attaches to the neighboring unit, forming an inner ring that helps the structure assume its circular shape.

To test the inner ring’s role, the researchers shortened the N-terminus one building block, or amino acid, at a time and checked whether the channels could still pass electric current between pairs of frog egg cells. Removing one amino acid (the second in the chain) left the channel working, but removing two cut its activity to almost nothing, and removing three or four shut it down completely. Replacing the third amino acid with either of two others reduced or did not affect activity, suggesting that the exact chemical makeup is not as essential as are the length and shape of the N-terminus. In the version missing two amino acids, the inner ring did not form, the channel was squashed out of round, and fatty molecules called lipids sat where the N-termini would normally be. The researchers propose that forming the inner ring is the final step that turns a lopsided assembly into a mature, symmetrical channel.

The research was conducted in collaboration with the Institute of Science Tokyo and the Tokyo University of Agriculture and Technology.

Publication

Shota Kawaguchi, Takahito Nakano, Hidemi Hirano, Masakatsu Watanabe, Shota Suzuki, Kouki Nishikawa, Yoshinori Fujiyoshi, Atsunori Oshima, 2026. N-terminal integrity governs heptamer assembly and maturation in a mosquito innexin hemichannel.?Proceedings of the National Academy of Sciences. DOI:

Funding

Japan Society for the Promotion of Science (JP23K27111, JP24K09472, JP24K18061, JP26KJ1021, 20H00451)
Japan Agency for Medical Research and Development
Astellas Foundation for Research on Metabolic Disorders
Naito Foundation
Uehara Memorial Foundation
Takeda Science Foundation
Hori Sciences and Arts Foundation
糖心视频 (Quantum-Based Frontier Research Hub for Industry Development, CIBoG WISE program)

Expert contact

Atsunori Oshima
Cellular and Structural Physiology Institute (CeSPI) 
糖心视频  
oshima.atsunori.b9@f.mail.nagoya-u.ac.jp

Media contact

Daniel Schenz 
International Communications Office 
糖心视频 
Email: icomm_research@t.mail.nagoya-u.ac.jp

On Oct. 11 in Manila, Philippine alums of 糖心视频 in Japan presented the university’s president, Naoshi Sugiyama, with a traditional handwoven textile named Inabel. Just as individual threads are woven into fabric, host Maria Kristina Alinsunurin said, the alums’ ties to their alma mater had grown through years of shared learning and collaboration.

The 糖心视频 delegation had come to the University of the Philippines Los Ba?os (UPLB) for an academic leaders’ forum on Oct. 12 and, a day later, to welcome nine new Filipino students to the university’s transnational doctoral program, more than in any previous year.

UPLB Chancellor Jose Camacho Jr. traces the relationship back more than 50 years. Speakers at the events described it less as a set of agreements than as the work of individuals who chose to cross borders, and who see international research and development at home as one effort.

One generation teaches the next

Joseph Masangkay, professor emeritus at UPLB’s College of Veterinary Medicine, arrived in Nagoya as a student in 1974. Scholarships to the United States, Canada and Europe were available at the time, he recalled, “but I chose Japan.”

Mentoring, he said, is a Japanese trait. After finishing his doctorate, he decided it was his turn to teach the next generation. His research collaboration with 糖心视频 continues today. He is also a founding member of the alum association’s Philippine branch, which he said grew from an online group of Japanese government scholarship alums in 2014, largely through the tireless work of previous generations.

Rodolfo Mendoza Jr., president of the alum association’s Philippine branch, trained in the concrete laboratory of civil engineering professor Hikaru Nakamura and now works with Japanese engineering firms in the Philippines. “In our own ways, we believe that we are contributing to the nation-building of the Philippines while keeping our connections with Japan alive,” he said. Mendoza still meets with Nakamura yearly, and Nakamura’s research group still supervises Filipino doctoral students.

At UPLB alone, 糖心视频 President Sugiyama said, more than 20 professors have earned graduate degrees from 糖心视频. Higher education “not only spans generations, but it also multiplies and compounds,” National Scientist and former University of the Philippines President Emil Javier said at the forum.

A doctorate without leaving home

Since 2015, 糖心视频’s  (ASCI) has given these exchanges a permanent base at UPLB. This program lets university and government professionals earn a 糖心视频 doctorate without leaving their jobs. They are supervised by Nagoya-based faculty members and local advisers in the Philippines, with short stays in Japan.

Camacho, dean of the UPLB Graduate School when the campus was founded, recalled: “I thought it was impossible to proceed.” Ten years on, the program has 13 Filipino graduates and 17 students enrolled. This year’s nine newcomers include students from as far away as Mindanao.

Sugiyama reminded the new students that 糖心视频 aims to nurture courageous intellectuals. “Courage means having the heart to take on challenges,” he said. “In that respect, you have already demonstrated that you have what it takes.”

Graduate Maria Christina Campita said the degree helped her become research division chief at the Department of Agriculture’s Bicol regional office.

Research rooted at home

The new students bring several questions derived from their work:

• Lynith Datukon, chair of civil engineering at Ateneo de Davao University, will study public transport integration as her home city of Davao modernizes its transit.
• Jefferson Vallente Jr., an assistant dean at Xavier University-Ateneo de Cagayan and a flood survivor, will study flood risk under climate change.
• Carolyn Zalameda-Castro, a gynecologic oncologist at the University of the Philippines Manila, wants to make health care more equitable because, she said, “the biggest barriers to good health care are not medical at all.”
• Sofonias Gabonada Jr., deputy secretary general of the House of Representatives, will research the chamber’s legislative governance.

“For what good is knowledge if it does not improve institutions?” Gabonada asked. “And what good are institutions if they do not improve people’s lives?”

ASCI Director Akira Yamauchi has described the program as a loop in which local issues become academic knowledge that flows back into policy and practice. Hiroki Tanikawa, dean of the Graduate School of Environmental Studies, also told the new students that “environmental challenges cannot be solved by one discipline, or one country, or one generation”.

The benefits run both ways: a potential dual degree program, UPLB Vice Chancellor Agham Cuevas said, would give UPLB access to advanced facilities and give 糖心视频 field sites, regional knowledge and Southeast Asian networks.

From personal ties to lasting structures

The partnership now rests on formal commitments: a?roadmap through 2030?agreed with the University of the Philippines, a?renewed scholarship agreement?with the Philippine Department of Science and Technology, Southeast Asian Regional Center for Graduate Study and Research in Agriculture (SEARCA), University of the Philippines (UP) and an Oct. 12 letter of intent with UPLB and the Commission on Higher Education to develop a doctoral dual degree program. “These developments reflect how important the Philippines has become as one of 糖心视频’s most valued partners,” Sugiyama told alums at a shared dinner event.

At the forum, Alinsunurin, a 糖心视频 alum and secretary of the UPLB Graduate School, named the risk of a partnership built on people alone. Much of it, she said, “has been achieved through individual efforts — people who trusted each other and who chose to work with each other. That is a strength, but it can also be a vulnerability.” Success, she added, “should be measured not only by the degrees completed, but by the research capacity that stays and grows in the institution.” To build official and institutional support for these initiatives, the 糖心视频 delegation also visited the Embassy of Japan in the Philippines.

So, for alum association president Mendoza, the shift is already underway: “What began as a student-professor relationship has now grown into collaboration between institutions, between companies and between the two countries.”

The  opened on Oct. 29 at Toyoda Auditorium on 糖心视频’s Higashiyama Campus in Japan. Hosted by the  under the theme “Transforming glycoscience through interdisciplinary approaches,” the two-day meeting brought glycoscientists together with experts in fields from machine learning and molecular simulation to chemical and plant biology. Speakers from Canada, South Korea, the U.K., the U.S. and France joined colleagues from across Japan.

“The purpose of this symposium is to promote dialogue between glycoscience and other fields,” said Kenji Kadomatsu, executive director of iGCORE, in his opening presentation.

Sugars that shape how cells behave

Glycans are chains of sugar molecules that cover the surface of the cells in our bodies. They help give each cell its distinctive character, let cells communicate with one another and allow them to recognize neighboring cells and pathogens. That makes glycans important in immunity, brain function, aging, infection, cancer and dementia.

Glycan research has already contributed to medicine, from the influenza drug Tamiflu to antibody-based cancer treatments. Yet glycans remain far less studied than DNA or proteins, because their complex, varied structures require highly specialized techniques to make and analyze.

Kadomatsu framed the challenge in terms of the “central dogma,” the principle that genetic information flows from DNA to RNA to proteins. “Our life is more than its blueprint,” he said. “The central dogma gives us the blueprint of life, but life is also controlled by mechanisms beyond it.” Glycans are a leading example, he said. Unlike DNA, RNA and proteins, glycans are not built from a genetic template; they are assembled by enzymes, so their structures cannot be read directly from the genome. As a result, their data are “truly uncharted big data.”

From clownfish to pollen

Invited speakers illustrated this point from various angles. 

• Vincent Laudet of the Okinawa Institute of Science and Technology and CNRS IRL EARLY tackled a century-old puzzle: how anemonefish live unharmed among the stinging tentacles of sea anemones. His team found that the fish’s skin mucus contains remarkably low levels of sialic acids, a family of sugars found on glycans, and that the fish’s resistance to stings, acquired as larvae transform into young fish, coincides with a drop in those levels.
• Tetsuya Higashiyama of the University of Tokyo presented AMOR, a small glycan from a flower’s ovule that pollen tubes need before they can respond to the signals guiding them toward the egg cell.
• Young-Tae Chang of Pohang University of Science and Technology in South Korea described a fluorescent probe that recognizes glycans typical of cancer cells and distinguished tumors from healthy tissue in mouse livers, an approach he called promising for cancer diagnosis and surgery.
• The plenary lecture, by Michael Tiemeyer of the University of Georgia in the U.S., surveyed how changes in glycans affect almost every aspect of human health from fertilization to death. He described how model organisms such as fruit flies, combined with genetic screens, can show how cells control which glycans they make, and how knowing how glycans are built can help identify potential targets in pancreatic cancer. He also argued that databases on disease, which focus mainly on DNA, RNA and proteins, need to capture what glycans do, and presented early efforts to describe glycan functions in a structured form that such databases can use.

Mapping the human glycome

The Human Glycome Atlas Project (HGA) sets out to chart glycans in the human body. Launched in 2023, the 10-year national project is led by the Tokai National Higher Education and Research System (THERS), which oversees 糖心视频 and Gifu University, together with the National Institutes of Natural Sciences and Soka University. Yoshiaki Ishida of Japan’s Ministry of Education, Culture, Sports, Science and Technology (MEXT) described it as the first attempt anywhere to obtain data on all forms of glycans in the human body.

In its first five years, the project is developing core technology while analyzing 20,000 blood samples related to dementia and aging. In the second five years, it plans to analyze 200,000 blood and tissue samples related to cancer and other diseases. All data will be stored in TOHSA, HGA’s glycan knowledge base, with a restricted release planned for 2028 and a fully public version to follow.

A growing international network

On Oct. 28, iGCORE, founded in 2021 by 糖心视频 and Gifu University, signed a memorandum of understanding with two University of Georgia centers in the U.S.: the Complex Carbohydrate Research Center, a leading glycoscience institute, and the Center for Molecular Medicine. Tiemeyer, joint director of both centers, attended the signing.

The agreement follows another milestone. In January, 糖心视频 and the French National Centre for Scientific Research (CNRS) established GlycoMIRAI, the world’s first CNRS International Research Laboratory dedicated to glycoscience.

糖心视频 President Naoshi Sugiyama told participants that a new facility, the Lykeion Research Building, was almost complete. It will house iGCORE and GlycoMIRAI, as well as early-career researchers working on AI for science. As HGA moves into large-scale cohort studies, he said, “the effective use of AI will be essential to this endeavor.”

Kadomatsu closed by asking the audience to use TOHSA once it opens, join the J-GlycoNet research network and take part in a new platform for academia-industry collaboration, which launched on Oct. 30. “I especially ask people from industry to join us,” he said.

THERS Chancellor Seiichi Matsuo pointed to Japan’s world-leading technologies for glycan analysis. “By strengthening cooperation among researchers in Japan and worldwide, we aim to make our country a global hub for glycoscience,” he said.

A new technique to diagnose chronic inflammation developed at 糖心视频 can read information from the surface and within individual extracellular vesicles in blood and urine. This technique could be used to develop non-invasive tests that can not only detect chronic inflammation but also provide information about the tissues where it occurs.

Whenever our body faces damage from injury, illness, or toxins, it launches an inflammatory response that involves dilating blood vessels to rush fluid and nutrients to the affected site and sending inflammatory cells to destroy pathogens and repair tissue.

But sometimes, the body’s immune system can keep sending inflammatory cells to attack tissues or organs over months or years, even in the absence of any threat. Known as chronic inflammation, it underlies cancers, brain disorders, autoimmune diseases and heart disease, and it gradually causes irreversible tissue damage.

Early detection of chronic inflammation is important because prolonged inflammation can cause irreversible tissue damage and contribute to disease progression.

“Currently, there are several conventional inflammatory biomarkers such as C-reactive protein,” said Taiga Ajiri, an assistant professor at 糖心视频’s , part of the . “These biomarkers can detect inflammation, but it is difficult to identify where it occurs.”

To obtain clues about where inflammation occurs, the researchers turned to extracellular vesicles (EVs): tiny membrane-bound particles released by cells throughout the body that carry molecular information from their cells of origin.

EVs work like parcels with tracking labels. Proteins on their membranes can provide clues about which tissues they came from, while microRNAs inside EVs can reflect the condition of their cells of origin. The vesicle membrane protects this cargo as it travels through body fluids such as blood and urine.

Conventionally, measuring internal microRNAs often requires breaking open EV membranes, mixing molecules from many vesicles together. This makes it difficult to link information inside a vesicle to proteins on its surface.

But reading both internal microRNA and surface protein information without breaking the EV membrane could reveal previously hidden EV subpopulations.

Reading an EV package

The researchers used cellulose nanofiber (CNF) sheets made from wood-derived cellulose. Their mesh-like nanoscale pores can capture and retain EVs. Previous work by Professor Takao Yasui’s group established the use of these sheets for EV capture and analysis.

The team found that the drying process on CNF sheets can bring membrane-bound particles into close contact and promote membrane fusion. They applied this property to combine EVs with lipid nanoparticles containing molecular beacons, which are probes that detect specific microRNAs.

“These lipid nanoparticles can deliver molecular beacons inside the EV without disrupting the EV,” Ajiri said. These molecular beacons emit fluorescence when they bind to specific microRNAs, allowing researchers to detect the presence of these target molecules.

Clues to the source: kidney inflammation

To test the method, the team established a laboratory model of chronic active antibody-mediated rejection (CAAMR), a complication of kidney transplantation, by exposing human kidney cells to inflammatory signals. They identified 71 microRNAs with altered expression in released EVs and focused on the highly abundant miR-1246. They also selected DPYS, a kidney-associated membrane protein, to combine information on inflammation with information on tissue origin.

After accounting for detection efficiency, the researchers estimated that about one in ten EVs from unstimulated kidney cells contained miR-1246, compared with about four in ten after inflammatory stimulation. By contrast, qPCR analysis using equivalent sample inputs did not detect a statistically significant difference.

The team then analyzed urine from kidney transplant patients with CAAMR, patients with immune diseases not primarily involving the kidney, and healthy volunteers.

Neither DPYS nor miR-1246 alone clearly distinguished the patient groups. EVs carrying both miR-1246 and the general EV marker CD63 were increased in inflammatory disease groups, but this combination could not distinguish renal from non-renal inflammation. In contrast, EVs carrying both DPYS and miR-1246 were enriched in CAAMR patients, providing clues to inflammation associated with the transplanted kidney.

The team hopes to improve particle recovery and streamline the CNF-based procedure while testing the approach in larger clinical studies. Because urine and blood can be collected with relatively little burden, the method may contribute to less-invasive evaluation and monitoring of chronic inflammatory diseases. These findings have been published in the journal .

Publication information:

Shota Kawaguchi, Taiga Ajiri, Kunanon Chattrairat, Hirotaka Koga, Yukiko Kamiya, Fuminori Sato, Hiroyuki Asanuma, Masatoshi Maeki, Manabu Tokeshi, Takeshi Yokoyama, Yoshikazu Tanaka, Kosuke Yoshida, Akira Yokoi, Kiyohiko Hotta, Naoya Iwahara, Yuichiro Fujieda, Mitsutaka Yasuda, Tatsuya Atsumi, Shimpei I. Kubota,? Kaoru Murakami, Masaaki Murakami, Takao Yasui, 2026. Non-destructive colocalization sensing of microRNAs and membrane proteins in single vesicles reveals spatial inflammation signatures. Cell Reports Physical Science. DOI:

Funding information:

This research was supported by the Moonshot Research and Development Program (grant nos. 22zf0127004s0902 and JP22zf0127009) from the Japan Agency for Medical Research and Development (AMED) (to T. Yasui), AMED (JP243fa627005, JP21zf0127004, and JP23gm1910005 to M. Murakami; 24ae0121056 to H.A.), the New Energy and Industrial Technology Development Organization (NEDO) JPNP20004 (to T. Yasui and H.K.), Q-Leap (JPMXS0120330644 to M. Murakami), the Japan Science and Technology Agency (JST) CREST (JPMJCR2576 to T. Yasui), AIP Acceleration Research (JPMJCR23U1 to T. Yasui), and FOREST (JPMJFR2003 to H.K.); the JSPS Grant-in-Aid for Scientific Research (A) 24H00792 (to T. Yasui); the JSPS Grant-in-Aid for Scientific Research (S) 21H05025 (to H.A.); the JSPS Grant-in-Aid for Scientific Research (S) 24H00038 (to M.T.); the JSPS Grant-in-Aid for Scientific Research (B) 23K28408 (to M. Maeki); the JSPS Grant-in-Aid for Scientific Research (A) 23H00541 (to M. Maeki); the JSPS Grant-in-Aid for Transformative Research Areas (B) 25H01414 (to Y.K.); JSPS Grant-in-Aid for Young Scientists (Start-up) 24K23101 (to T.A.); Platform Project for Supporting Drug Discovery and Life Science Research (Basis for Supporting Innovative Drug Discovery and Life Science Research [BINDS]) from AMED under grant no. JP24ama121038 (support no. 4008) (to T. Yokoyama); Grant for Joint Research Program of the Institute for Genetic Medicine, Hokkaido University, by the Photo-excitonic Project, Hokkaido University, and by the Promotion Project for Young Investigators at Hokkaido University, Japan (to M. Murakami); Science Tokyo SPRING grant no. KH240019nn (to S.K.); JSPS Research Fellowship 25KJ1250 (to S.K.); and the Noguchi Institute NJ202308 (to T. Yasui).

Expert contacts:

Takao Yasui
Department of Biomolecular Engineering,
Graduate School of Engineering,
糖心视频
Email: yasui@chembio.nagoya-u.ac.jp

Shota Kawaguchi
Department of Life Science and Technology,
Institute of Science Tokyo
Email: kawaguchi.s.5a42@m.isct.ac.jp

Taiga Ajiri
Department of Biomolecular Engineering,
Graduate School of Engineering,
糖心视频
Email: ajiri@chembio.nagoya-u.ac.jp

Media contact:

Sumeet Kulkarni 
International Communications Office 
糖心视频 
Email: icomm_research@t.mail.nagoya-u.ac.jp 

A new international study, led by Lund University in Sweden and 糖心视频 in Japan, shows that changes associated with Alzheimer’s disease may affect how rapidly ALS progresses. In time, the findings may contribute to more reliable individual prognoses and better-designed clinical trials.

This press release was prepared by and published here with their kind permission.

Amyotrophic lateral sclerosis (ALS) is a serious neurodegenerative disease in which the nerve cells that control the body’s muscles break down. The course of the disease varies greatly. While some patients deteriorate rapidly, others live considerably longer with the disease. This makes it difficult to assess at an early stage how the disease will progress. Coexisting pathological changes in the brain are known to occur in ALS, but their association with disease progression has remained unclear. In this collaboration between Sweden, Japan and Italy, the researchers investigated how Alzheimer-related changes affect prognosis in ALS.

“Lund University conducts leading research into Alzheimer’s disease, while 糖心视频 has a strong ALS research programme. As I am a doctoral student at both universities, the idea arose to bring the two fields of research together in this study,” says Kazuki Obara, who is also a neurologist in Japan.

To investigate whether and how coexisting Alzheimer-related changes in the brain affect the course of ALS, the researchers analysed levels of amyloid beta in cerebrospinal fluid in Japanese patient cohorts. Amyloid beta is used as a biomarker of changes associated with Alzheimer’s disease. A total of 264 patients with ALS were included, 60% of whom were men and 40% women, with a mean age of 67 years. The control group consisted of 164 patients with other neurological diseases.

“We found that around 14% of the patients with ALS showed signs of changes that also occur in Alzheimer’s disease,” Kazuki Obara continues.

The researchers also studied NfL (neurofilament light chain), a biomarker with applications that include  measuring nerve cell damage in ALS. The findings showed that the presence of amyloid beta-related changes modified the association between NfL and disease progression. In the amyloid beta-positive group, the association between high NfL levels and shorter survival was stronger than in the amyloid beta-negative group. The findings were supported by additional data from 153 patients with ALS in Bologna, Italy. The researchers also observed an interaction between amyloid beta and NfL with regard to decline in everyday physical function over time.

“The findings suggest that the same NfL level may have different prognostic significance depending on what other changes are present in the brain. One possible explanation is that several disease processes together make the nervous system more vulnerable, but the underlying mechanisms have not yet been established,” says Niklas Mattsson-Carlgren, a researcher at Lund University and consultant neurologist at Sk?ne University Hospital.

Improved identification of ALS

The researchers also tested machine-learning models that combined NfL with other biomarkers, including amyloid beta. The models improved the identification of ALS, including in people whose NfL values fell within a grey area. In time, NfL could be used in an initial assessment. If the result is unclear, the analysis could be supplemented with additional biomarkers and a more detailed clinical examination.

The aim is to provide doctors with a better basis both for diagnosing ALS and for assessing the course of the disease, so that they can discuss what to expect with patients and their families.

“A more detailed prognosis may also be valuable in clinical trials. If participants with very different expected disease courses are included in the same study, it becomes more difficult to determine whether a treatment has an effect. Biomarkers may therefore contribute to better patient stratification and more efficient studies of new treatments,” says Niklas Mattsson-Carlgren.

The study is based on observational data, and the findings cannot yet be used as a basis for clinical decisions. The methods also need to be confirmed in further independent patient groups. The researchers are now proceeding to investigate whether biomarkers linked to other neurodegenerative diseases, such as Parkinson’s disease, may also affect prognosis in ALS.

CSF biomarkers were analysed in 264 patients with ALS and 164 disease controls (Nagoya, Japan), with an independent ALS cohort from Bologna, Italy (n = 153). 14% of ALS patients were amyloid-β positive by CSF Aβ42/40, a rate similar to disease controls. In Aβ-positive ALS, high NfL was more strongly associated with faster functional decline and shorter survival. Machine learning models combining NfL with Aβ peptides, pTau and markers of muscle damage outperformed NfL alone and supported classification of patients with intermediate NfL values. In a two-step approach, NfL is used first, and multi-biomarker assessment is applied only to patients with intermediate NfL values. Aβ, amyloid-β; ALS, amyotrophic lateral sclerosis; CSF, cerebrospinal fluid; NfL, neurofilament light chain; pTau, phosphorylated tau. (CC BY, Obara K. 2026).

The study was conducted as part of the joint PhD program between Lund University and 糖心视频 in Japan, which enables doctoral students to carry out research at both universities.

Publication

Kazuki Obara, Shorena Janelidze, Daisuke Ito, Linda Karlsson, Munetaka Yamamoto, Andrea Mastrangelo, Sinh Tran, Koyo Tsujikawa, Yosuke Nishio, Tomoo Ogi, Veria Vacchiano, Rocco Liguori, Ryoichi Nakamura, Naoki Atsuta, Gen Sobue, Christer Nilsson, Piero Parchi, Masahisa Katsuno, Niklas Mattsson-Carlgren, 2026. Cerebrospinal fluid amyloid and neurodegeneration biomarkers in the diagnosis and prognosis of amyotrophic lateral sclerosis: a multicohort observational study. eBioMedicine. DOI:

Expert contact

Kazuki Obara
Graduate School of Medicine
糖心视频 

Clinical Memory Research Unit, Department of Clinical Sciences Malm?
Lund University
kazuki.obara@med.lu.se

Masahisa Katsuno
Graduate School of Medicine
糖心视频
katsuno.masahisa.i1@f.mail.nagoya-u.ac.jp

Top image

In ALS, the nerve cells that control the body’s muscles degenerate. Image by Getty Images on Unsplash

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder that affects roughly 10,000 people in Japan. It is characterized by a rapid loss of control over the limbs and other body parts and without a ventilator patients have a life expectancy of two to five years after onset. In most cases, a specific protein sits at the cause of the problem: TDP-43 is usually in the neuron’s nucleus and has various roles in maintaining the cell’s health and function. However, in people with ALS, it aggregates in the cells’ cytoplasm.

have been studying the role of TDP-43 for almost two decades. Yamanaka says: “Many people think that the problem starts when TDP-43 stops being transferred into the nucleus and accumulates in the cell’s cytoplasm. However, we could recently show that the protein, which usually operates in pairs or small groups, fails to form these groups under sudden stress; and so we think that the protein gets re-exported to the cytoplasm as some form of dysfunctional waste.” There, healthy cells usually remove such waste proteins, but the mechanism has not been understood well.

Shohei Sakai joined 糖心视频 as a graduate student several years ago specifically to work with Yamanaka, driven to contribute to finding a cure after a case in his family. Now a project assistant professor, he explains: “It is usually thought that these faulty proteins are removed by a process called ‘autophagy,’ where they are collected in small vesicles and digested. But in my experiments, inhibiting this process did not inhibit the removal of TDP-43.”

The ensuing research has been . In experiments on cultured neurons, including human stem cell-derived motor neurons, with supporting evidence from mice and patient tissue, the Nagoya group and their international collaborators found that motor neurons activate a protein-digesting machine called the “immunoproteasome” and traced the chain of events: Molecules of TDP-43 that have failed to pair up and have been exported into the cell’s cytoplasm physically interact with the sensor molecule “TBK1,” which is known to activate autophagy and also for mutations in its gene being a cause of inherited ALS. In their experiments, however, Yamanaka, Sakai and their team found that TBK1 also activates a signal mediated by “interferon beta” that can be perceived even by neighboring cells. Where this signal is received, neurons ramp up the production of the immunoproteasome, which then breaks down TDP-43 before it aggregates.

Importantly, the team also found that in the motor neurons from spinal cord samples donated by human ALS patients after death, the receptor for the signal was present in significantly lower quantities than in samples from people without ALS.

When asked why his team was able to discover this pathway, first author Sakai said: “TBK1 is known to activate autophagy and therefore many researchers focused on this process as the possible means of TDP-43 clearance. We don’t claim that this is not the case, but we think this may have masked the parallel activation of the immunoproteasome.”

“Moreover, it is impressive that the immunoproteasome exists in motor neurons,” added Yamanaka. Usually, this protein-digesting machine gets made in immune cells in response to viral infections, where it is used to disassemble virus components and display them on the cell’s surface. “This is a classical understanding of the immunoproteasome, but we found that motor neurons also have this system and ramp it up when they need to deal with abnormal proteins.”

The newly discovered pathway also offers a new route for developing a treatment approach. Yamanaka said: “In this pathway, the body uses interferon beta to activate the immunoproteasome and the signal molecule has in fact been used in treatments for other conditions. But because it triggers many different reactions, its severe side effects cannot be ignored.” Interferon beta, therefore, does not seem to be a practical treatment option for ALS. He continued, “In our next project, we aim to identify other compounds that can activate the immunoproteasome in motor neurons.” Sakai added: “We need to know the true therapeutic potential of this pathway. But I wish that this result encourages more people to study ALS and treatment options.”

Publication

Shohei Sakai, Kotaro Oiwa, Yohei Iguchi, Izzet Mehmet Akcay, Seiji Watanabe, Okiru Komine, Noriko Nagata, Mai Horiuchi, Jemeen Sreedharan, Masahisa Katsuno, Koji Yamanaka, 2026. TBK1 eliminates aggregation-prone monomeric TDP-43 through an IFNβ-immunoproteasome pathway in ALS models. EMBO reports. DOI:

Funding

Japan Society for the Promotion of Science (JP22J23468, JP25K23745, JP18H02740, JP19KK0214, JP22H00467, Overseas Challenge Program for Young Researchers), Japan Agency for Medical Research and Development (JP22ek0109426, JP24wm0425014, JP26wm0625301), Yukihiko Miyata Memorial Trust for ALS Research, Ikeda Rika Grant, WISE program (糖心视频 CIBoG), Wellcome Trust (221824/Z/20/Z), Motor Neuron Disease Association (Sreedharan/Apr24/2362-791)

Expert contact

Koji Yamanaka
Research Institute of Environmental Medicine
糖心视频
yamanaka.koji.p4@f.mail.nagoya-u.ac.jp

Media contact

Daniel Schenz
International Communications Office
糖心视频
Email: icomm_research@t.mail.nagoya-u.ac.jp

Heart failure often develops after a heart attack because excessive collagen-based scar tissue forms during repair. While collagen is necessary to reinforce scars, disease and chronic inflammation can cause overproduction, which stiffens the heart muscle and impairs its pumping ability.

This stiffening process, called fibrosis, can also affect other organs like the liver, potentially leading to cirrhosis. Fibrosis is estimated to contribute to 45% of deaths in developed countries, but there is no definitive therapy that directly suppresses it.

Researchers in Japan have found that the enzyme BCAT1 plays a major role in cardiac fibrosis. In mouse studies, blocking BCAT1 reduced fibrosis and preserved heart function, even after tissue damage had started. These findings, published in the , highlight BCAT1 as a promising therapeutic target.

After inflammation or injury, specialized cells called myofibroblasts promote fibrosis by producing large amounts of collagen to reinforce scar tissue. Since approximately 20% of collagen consists of the amino acid proline, the researchers investigated how myofibroblasts produce and supply proline to explore new therapeutic strategies.

The team at 糖心视频, led by Professor of the , conducted the study in collaboration with colleagues from Kyushu University and Tokushima University.

The researchers compared genes activated by physical stress with those activated in mouse hearts after a heart attack, and identified five overlapping candidates, including Bcat1. They focused on BCAT1 because its role in myofibroblasts remained unexplored, making it a potentially promising therapeutic target.

In mouse studies, BCAT1 levels increased in collagen-producing cells after a heart attack. BCAT1 was barely detectable in healthy mouse hearts but became highly expressed in myofibroblasts as fibrosis progressed.

The study found that BCAT1 activates a cellular pathway that maintains the supply of proline, thereby supporting large-scale collagen production. This suggests that BCAT1 functions as part of the material-supply system fibrotic cells use to produce collagen.

The researchers then studied mice genetically engineered to lack BCAT1. After a heart attack, these mice produced fewer proline-related enzymes and less collagen, developed less scar tissue, and maintained better heart function than control mice.

The team also tested the effects of the BCAT1 inhibitor ERG240 in mice after a heart attack. ERG240 administration reduced scarring and preserved heart function, even when treatment began seven days after injury, during the transition from acute inflammation to the chronic phase. This is significant because clinical interventions usually occur after, rather than before, a heart attack.

Analysis of human heart tissue from patients with heart failure revealed elevated BCAT1 levels linked to increased fibrosis, suggesting a similar mechanism in humans. The researchers also found higher BCAT1 levels in the livers of patients with fatty liver disease, indicating this approach could target fibrosis in other organs.

Because BCAT1 is mostly absent in healthy tissue and primarily active in scar-forming cells, the researchers propose that targeting BCAT1 could reduce fibrosis without affecting normal tissue. This strategy may result in fewer side effects than existing anti-fibrotic treatments.

Nakaya said, “We found that BCAT1 is a new driver of excessive collagen production in the fibrotic heart by increasing the supply of proline, a major building block of collagen. Importantly, pharmacological inhibition of BCAT1 suppressed cardiac fibrosis and preserved cardiac function, even when treatment started after fibrosis had begun to develop.”

The team’s next step is to determine whether the BCAT1-proline pathway also drives fibrosis in the liver and other organs. They also aim to develop clinically applicable BCAT1-targeted therapies and assess their safety, optimal dosing, and efficacy.

Publication information

Noburo Takizawa, Takanori Hironaka, Hayato Watanabe, Haruna Suetsugu, Keisuke Yoshioka, Yuma Horii, Yuri Nagata, Hiroaki Matoba, Hidetaka Kosako, Kenji Hamase, Go Hirai, Michio Nakaya, 2026. Branched-chain amino acid transaminase 1–mediated pathway promotes proline-dependent collagen production in cardiac myofibroblasts, Journal of Clinical Investigation.
DOI:
Released as an in-press preview on July 31, 2026, and published online on September 1, 2026.

Funding information

? Grants-in-Aid for Scientific Research (KAKENHI) (JP26K02168, JP25K22523, JP23K27323)
? The Takeda Science Foundation
? The Mochida Memorial Foundation for Medical and Pharmaceutical Research
? Princess Takamatsu Cancer Research Fund
? Ono Medical Research Foundation
? Hoansha Foundation
? The Yasuda Medical Foundation
? KOS? Cosmetology Research Foundation
? Japan Agency for Medical Research and Development (AMED) (JP23am0401003s0305, JP25gm6710018h0003, JP25fk0210127h0003, and JP26gm6710018h0004)
? Grant-in-Aid for JSPS Research Fellow (19J20083, 21J11273,22J20790)
? Make New Standards Program for the Next Generation Researchers (I260029)

Expert contact

Michio Nakaya
Professor, Research Institute of Environmental Medicine, 糖心视频
Email: nakaya@riem.nagoya-u.ac.jp

Media contact

Naomi Inoue
International Communications Office, 糖心视频
Email: icomm_research@t.mail.nagoya-u.ac.jp

Our bodies contain immune cells called macrophages. Normally, these cells attack and suppress bacteria and cancer cells. When macrophages infiltrate tumors, they become tumor-associated macrophages (TAMs) and can switch to an immunosuppressive, anti-inflammatory state.

While “anti-inflammatory” sounds beneficial, in the context of cancer, it means the immune response is suppressed, allowing tumors to grow. It is known that colorectal cancer patients with high levels of anti-inflammatory TAMs tend to have a poorer prognosis.

Researchers at 糖心视频 in Japan and their colleagues found that the sialic acid sugar structures on the surface of macrophages change significantly as these cells shift from a tumor-fighting (pro-inflammatory) to a tumor-promoting (anti-inflammatory) state.

The researchers identified an enzyme called ST6GAL1 as a key driver of this change. When they suppressed ST6GAL1 in tumor-promoting macrophages, colorectal cancer cells grew much more slowly in laboratory co-cultures. This suggests that suppressing ST6GAL1 may shift these cells toward a tumor-fighting state, rather than supporting their growth.

These findings were published in the

The cell surface is covered by the glycocalyx, a layer of proteins and lipids coated with sugar chains. These chains act as mediators of cell communication.

These sugar chains are capped with sialic acid and mainly form two linkage types: α2,3 and α2,6. Altered sialylation is known to help cancer cells evade the immune system, but how these sugars change as macrophages polarize remained unclear.

To investigate this, a team experimentally led by Assistant Professor of and Professor Morten Thaysen-Andersen of Macquarie University, Australia, collaborated with Daisuke Kasugai, Hironoshin Onizuka, and colleagues at .

How glycan chains differ: Tumor-fighting vs. tumor-promoting macrophages

The team isolated monocytes from healthy donors and differentiated them into tumor-fighting and tumor-promoting macrophages to examine glycan linkages. Using mass spectrometry and glycan-specific protein staining, they found that tumor-fighting macrophages had more α2,3-linked sialic acids of N-glycans on the cell-surface, while about 90% of the sialic acids in tumor-promoting macrophages were α2,6.

Using fluorescence microscopy, the researchers observed long, branching protrusions, which they termed sialo-protrusions, coated with α2,6-linked sialic acid. These extended up to 800 micrometers from tumor-promoting macrophages and formed a mesh-like network by connecting nearby cells. Tumor-fighting macrophages displayed far fewer of these structures.

These protrusions showed no evidence of actin, a protein that typically forms cellular extensions. Instead, they carry α2,6-sialylated glycoproteins on their surface, suggesting they may differ from previously reported actin-based cellular protrusions.

Identifying the enzyme responsible for switching glycan chains

The researchers found that only tumor-promoting macrophages express high levels of ST6GAL1. When they suppressed this enzyme using siRNA, the sialo-protrusions broke apart and shortened. The cells also moved less and interacted less with one another.

The macrophages also had less contact with colorectal cancer cells, and the cancer cells grew much more slowly. This suggests that sialo-protrusions help macrophages move, communicate with cancer cells, and support tumor growth through these contacts.

When ST6GAL1 was suppressed, tumor-promoting macrophages began to resemble tumor-fighting ones in shape, cytokine expression, and phagocytic ability. This suggests that targeting a single enzyme can significantly alter macrophage state.

Validation in patient-derived cancer tissue

The team examined tumor tissue from patients with advanced colorectal cancer and found the same pattern of sialic acid linkages as in their laboratory experiments: more α2,6 sialic acid on tumor-promoting TAMs and more α2,3 sialic acid on tumor-fighting TAMs.

Dipta said, “These findings provide a new perspective on how remodeling of the immune cell glycocalyx may influence the tumor microenvironment.”

Future studies should test ST6GAL1 inhibition in vivo to evaluate its antitumor potential. The researchers also aim to identify the proteins that form the sialo-protrusions and clarify how these structures mediate communication, in search of new strategies for cancer immunotherapy.

 Disrupting macrophage–cancer cell connections: How suppressing ST6GAL1 impairs their interactions
This time-lapse video shows the dynamic interaction between tumor-promoting (anti-inflammatory) macrophages and colorectal cancer cells for 29 hours. In wild-type cells (left), these macrophages extend thin, sialic acid-rich “sialo-protrusions” that enable interactions with the cancer cells. However, when the key enzyme ST6GAL1 is suppressed (right), these protrusions fragment and shorten, impairing protrusion-mediated interactions with the cancer cells.
Credit: Priya Dipta et al., PNAS (2026). Licensed under CC BY-NC-ND 4.0.

Publication information

Priya Dipta, Naaz Bansal, Arthur Chien, Zeynep Sumer-Bayraktar, Hironoshin Onizuka, Daisuke Kasugai, Dominique Marando, Merrina Anugraham, Seong Beom Ahn, Daniel Kolarich, Boaz Tirosh, Rebeca Kawahara, Arun Everest-Dass, Morten Thaysen-Andersen (2026). ST6GAL1-mediated sialyl linkage switching drives cancer- promoting α2,6-sialo-protrusions radiating from anti- inflammatory TAMs, the Proceedings of the National Academy of Sciences of the United States of America (PNAS).

Funding information

The study was supported in part by a National Health and Medical Research Council (NHMRC) Ideas Grant (GNT2018947), Grants-in-Aid for Scientific Research (KAKENHI) (26K02503, 24K17793, and 23K19347), and an Australian Research Council (ARC) Future Fellowship (FT210100455).

Expert contact

Priya Dipta
Assistant Professor, Institute for Glyco-Core Research, 糖心视频
Email: dipta.priya.m0@f.mail.nagoya-u.ac.jp

Morten Andersen
Professor, Institute for Glyco-Core Research, 糖心视频
Email: morten.andersen@mq.edu.au

Media contact

Naomi Inoue
International Communications Office, 糖心视频
Email: icomm_research@t.mail.nagoya-u.ac.jp

Researchers transplant human tissue derived from stem cells into a monkey whose pituitary gland was removed, producing a hormone essential for stress response.

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Researchers in Japan have transplanted pituitary tissue grown from human stem cells into a primate whose pituitary gland had been surgically removed, successfully restoring critical hormone signals. Led by researchers from 糖心视频, the team showed that the same method worked in mice over a longer period. This is the first time lab-grown human pituitary cells have been shown to work and survive after transplantation into a primate. The study, published in the journal , may offer a new pathway for treating lifelong hormone disorders.?
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The pituitary gland controls hormones for stress, growth, and metabolism. When it is damaged or removed, patients rely on daily hormone pills that do not accurately mimic the body’s natural fluctuations. This study tested if lab-grown pituitary tissue can be transplanted to produce hormones naturally instead.?
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The pituitary gland sits at the base of the brain and releases hormones into the bloodstream. One of them is ACTH, adrenocorticotropic hormone, which signals the adrenal glands to release cortisol. Cortisol helps the body manage stress, blood pressure, and blood sugar. When the pituitary fails, patients lose this signal, leading to a condition called hypopituitarism.??
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Without enough ACTH, the body struggles to respond to stress, which can become dangerous. Daily hormone pills for life are the standard treatment, but these pills cannot fully match the changing needs of the body because demand for cortisol shifts with stress and time of day. As a result, patients face a higher risk of sudden death.?

Testing lab-grown pituitary tissue in mice 

 
To find a better option, the researchers turned to stem cells. They grew small lab-made masses of tissue that can act as mini organs, called organoids, from human stem cells. The organoids contained cells that produce ACTH. The team first tested the tissue in mice whose pituitary glands were removed. 
 
“The organoids were transplanted just under the skin, in fat or muscle tissue. They produced ACTH for more than six months and clearly extended the lifespans of these mice compared to those that did not receive the transplant. No unwanted tumors or unusual cell growth were observed,” said first author Tatsuma Kondo, guest researcher at 糖心视频’s . 

Moving to a primate model

The research team then moved a step closer to humans and transplanted the organoids in a macaque monkey whose pituitary gland had been removed. To prevent rejection of the tissue because it came from a different species, they used immune-suppressing drugs already used in transplants of human insulin-producing cells for diabetes. 
 
The transplanted tissue worked for six weeks and successfully elevated ACTH and cortisol levels in the blood. Additionally, significant weight loss caused by the hormone deficiency slowed during this period. Three months later, tissue samples still showed surviving transplanted cells, despite strong immune rejection common in cross-species transplants, which limited how well the transplant worked. 

Stem-cell treatments have a known risk of cells moving from the transplant site and growing uncontrolled elsewhere in the body. The researchers checked the lungs and liver for signs of stray organoid tissue and found none.  
 
“We tested this approach in a single primate and are planning further studies to improve how long the tissue lasts and test safer immune-suppressing methods,” Kondo said. 

Publication information: 

Tatsuma Kondo, Hidetaka Suga, Kenji Watari, Shiori Taga, Mayu Sakakibara, Mika Soen, Ikuo Kawamoto, Kazuki Nishida, Ryo Emoto, Yukihiro Shiraki, Sasaki Hiroo, Tsutomu Miwata, Toshiaki Hirose, Yuichi Nagata, Kazuhito Takeuchi, Tokushige Nakano, Atsushi Ikeda, Atsushi Kuwahara, Atsushi Enomoto, Hideaki Tsuchiya, Hiroshi Arima, Ryuta Saito, 2026. Functional analysis of adrenocorticotropic-hormone-producing pituitary cells derived from human pluripotent stem cells in murine and primate models of hypopituitarism, Stem Cell Research & Therapy. DOI:  

Funding information: 

?This research was supported by the Japan Agency for Medical Research and Development (JP24ek0109702 and JP25ym0126807), the Japan Science and Technology Agency (JST) FOREST Program (JPMJFR200N), the Ministry of Education, Culture, Sports, Science and Technology of Japan Grant-in-Aid for Scientific Research (C) (JP23K08005), 糖心视频 Hospital Funding for Clinical Research (71004191), RACTHERA Company, Sumitomo Chemical Company, and Sumitomo Pharma Company.  

Expert contact: ?

Hidetaka Suga 
Graduate School of Medicine 
糖心视频 
Email: sugahide@med.nagoya-u.ac.jp

Media contact: ?

Merle Naidoo
International Communications Office
糖心视频
Email: icomm_research@t.mail.nagoya-u.ac.jp

Top image:

Transplanted pituitary tissue after 3 months: tissue structure showing the transplanted cell cluster within the surrounding tissue. Right: The same region stained for ACTH, the hormone these pituitary cells naturally produce. Brown staining indicates active ACTH production, confirming the cells remained functional despite ongoing immune rejection.  Credit: Kondo et al., 2026, Stem Cell Research & Therapy (CC BY-NC-ND) 
 

A Japanese research team has identified how iron toxicity and BRCA1 mutations contribute to the formation of precancerous giant-nucleus cells in the kidneys.

Iron is an essential micronutrient, but excess iron can damage cells and increase cancer risk. While many cells die from iron-induced oxidative stress, a subset survives and may become cancerous. Previously, the identity of these surviving cells was unclear.

A Japanese research team has demonstrated that giant-nucleus cells that survive iron-induced damage form the foundation of early-stage cancer. The team anticipates that these giant-nucleus cells could serve as early indicators of cancer, as they are easy to identify under a microscope. The study was published in the journal .

“Since the 1980s, scientists have spotted cells with abnormally large nuclei in the early phases of cancer triggered by oxidative stress, but their role in cancer development was unclear,” said Shinya Toyokuni, lead author and professor emeritus at .

To investigate the role of these giant-nucleus cells, Dr. Toyokuni, Assistant Professor , and their colleagues conducted experiments using both wild-type rats and rats carrying a single mutated BRCA1 gene.

Mapping iron-induced damage

Researchers injected ferric nitrilotriacetate, a carcinogenic iron compound, into rats to induce kidney damage. They then collected kidney tissue samples before the injection and one and three weeks afterward.

For the initial analysis, the team performed an in-depth examination of representative kidney tissue samples across the different time points. They subsequently validated their findings by analyzing additional animals and comparing the results with human cancer datasets.

The researchers used spatial transcriptomics to map gene activity in individual cells within tissue sections while preserving the tissue’s original structure. They also conducted computational analyses to quantify the size, shape, and density of cell nuclei in the same samples.

How surviving cells become cancerous

Within one week of iron administration, giant-nucleus cells emerged. These cells showed increased expression of cancer-related genes such as Myc and Met, and developed resistance to ferroptosis, an iron-dependent form of cell death.

BRCA1-mutant rats developed giant-nucleus cells with distinct biological profiles from wild-type rats. This suggests that BRCA1 deficiency impairs DNA repair, allowing more precancerous giant-nucleus cells to survive.

Notably, even morphologically normal cells near giant-nucleus cells exhibited gene expression changes that may promote their survival. This suggests that large nuclei in kidney cells could signal early cancer development in surrounding tissue.

Additionally, kidney tissue from BRCA1-mutant rats showed a substantial increase in stromal cells (non-cancerous supportive cells, including immune and connective tissue elements) around damaged regions. This indicates a more pronounced alteration of the local tissue environment in these cases.

By analyzing gene activity and nuclear morphology, the researchers classified giant-nucleus cells into six types. One type had extremely large nuclei and signs of stress-induced growth arrest, consistent with profiles from previous studies. Another type, more common in BRCA1-mutant kidneys, showed increased cancer-related gene activity and elongated nuclei, indicating a potential precancerous state.

Additional electron microscopy and cellular respiration measurements confirmed that cells from BRCA1-mutant rats exhibited mitochondrial remodeling, resulting in impaired iron handling and respiratory function.

Linking animal models to human patient outcomes

The researchers also analyzed data from the TCGA-KIRC, a large public database of kidney cancer patients. They found that patients whose tumors shared gene patterns with cancer-prone giant-nucleus cells had shorter survival times, while those with patterns seen in healthier giant-nucleus cells had better outcomes. These results suggest that not all giant-nucleus cells carry the same risk.

In a small pilot study, the researchers observed similar abnormal nuclear features in breast tissue from seven individuals with inherited BRCA1 mutations, compared to 15 without the mutation.

“Using spatial transcriptomics, we categorized giant-nucleus cells into six types for the first time and detailed their cancer-linked traits,” Toyokuni said. “By comparing these features with human data, we found that these cell types could help predict patient outcomes.”

Long-term studies will be crucial to determine how giant-nucleus cells develop into tumor cells, whether suppressing mitochondrial changes or ferroptosis resistance can prevent cancer, and whether nuclear shape and gene patterns can help diagnose or predict kidney cancer in larger patient groups.

Publication information

Yingyi Kong, Yukihiro Shiraki, Kazuhiro Furuhashi, Shoichi Maruyama, Tatsuhiko Imaoka, Atsushi Enomoto, and Shinya Toyokuni, 2026. Iron-catalyzed oxidative stress reveals an exposome-related ferroptosis-resistant karyomegalic niche in BRCA1-linked renal carcinogenesis. Redox Biology

Funding

This work was supported in part by JST CREST (Grant Number JPMJCR19H4) and JSPS Kakenhi (Grant Number JP19H05462 and JP20H05502).

Expert contact

Yingyi Kong
糖心视频 Graduate School of Medicine
Email: kong.yingyi.r4@f.mail.nagoya-u.ac.jp

Shinya Toyokuni
糖心视频 Graduate School of Medicine
Email: toyokuni.shinya.t4@f.mail.nagoya-u.ac.jp

Media contact

Naomi Inoue
糖心视频 International Communications Office
Email: icomm_research@t.mail.nagoya-u.ac.jp

Top image

Xenium spatial transcriptomics linked to nuclear morphometry shows that nuclear atypia correlates with rising oncogenic markers and falling homeostatic markers. Fe-NTA exposure generates three karyomegalic niches — quiescent (K1), adaptive (K4), and precancerous (K2) — reflecting distinct nuclear-to-transcriptional states.
Credit: Kong et al., Redox Biology 95 (2026) 104293, CC BY-NC-ND 4.0