Stem Cell ReportsPub Date : 2026-09-08Epub Date: 2026-08-27DOI: 10.1016/j.stemcr.2026.103060
Xiaole Tong, Marieke Visscher, Frank M Riemers, Danielle Versluis, Niels Geijsen, Peng Shang, Marianna A Tryfonidou, Deepani W Poramba-Liyanage
{"title":"CRISPR activation reveals SOX5/6/9 as key transcriptional regulators directing iPSC-derived cells toward a notochordal lineage.","authors":"Xiaole Tong, Marieke Visscher, Frank M Riemers, Danielle Versluis, Niels Geijsen, Peng Shang, Marianna A Tryfonidou, Deepani W Poramba-Liyanage","doi":"10.1016/j.stemcr.2026.103060","DOIUrl":"10.1016/j.stemcr.2026.103060","url":null,"abstract":"<p><p>Intervertebral disc (IVD) degeneration, a leading cause of chronic lower back pain, is associated with loss of vacuolated notochordal cells (NCs) and fibrotic remodeling of the nucleus pulposus. Emerging therapies increasingly focus on NCs, which are rare but therapeutically relevant cells for regenerating degenerated IVDs. In this study, we used CRISPR-based transactivation (CRISPRa) to direct the differentiation of human induced pluripotent stem cells (iPSCs) into the NC lineage. We tested CRISPRa-mediated activation of NOTO, TBXT, FOXA2, SOX5, SOX6, and SOX9, coupled with single-cell sequencing of Aggrecan-2A-mScarlet reporter iPSCs. This approach identified the SOX5/6/9 combination (SOX-trio) as critical for promoting NC lineage commitment. The SOX-trio yielded the largest cell population expressing a range of genes previously associated with NC identity, including SHH, FOXA1, FOXA2, FOXJ1, FN1, ALCAM, KRT8, and KRT18. Our study demonstrates the integration of CRISPRa with single-cell technologies as a powerful platform for investigating and enriching iPSC-derived NCs, supporting future regenerative strategies across various fields.</p>","PeriodicalId":21885,"journal":{"name":"Stem Cell Reports","volume":" ","pages":"103060"},"PeriodicalIF":5.6,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13555567/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148841104","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Stem Cell ReportsPub Date : 2026-09-08Epub Date: 2026-08-20DOI: 10.1016/j.stemcr.2026.103050
Theodore E Ewachiw, Tenaya K Vallery, Shloka Dhar, Hayden Clarkson, Tiffany Elston, Haileigh Gay, Bradley B Olwin
{"title":"TDP-43 sustains satellite cells to maintain and regenerate skeletal muscle.","authors":"Theodore E Ewachiw, Tenaya K Vallery, Shloka Dhar, Hayden Clarkson, Tiffany Elston, Haileigh Gay, Bradley B Olwin","doi":"10.1016/j.stemcr.2026.103050","DOIUrl":"10.1016/j.stemcr.2026.103050","url":null,"abstract":"<p><p>Skeletal muscle satellite cells (SCs), residing between the myofiber plasma membrane and the surrounding basement membrane, continue to maintain and repair skeletal muscle throughout life. Typically, quiescent SCs can transition into a reversible alert state (G<sub>Alert</sub>) that primes them for rapid activation to maintain or repair muscle. From G<sub>Alert</sub>, SCs can either re-enter quiescence or commit to the cell cycle, expand, and differentiate to fuse with existing regenerating myofibers. Exit from quiescence requires extensive post-transcriptional remodeling, including changes in RNA processing and RNA-binding protein activity. We show that TDP-43, an RNA-binding protein, is essential for SC maintenance and muscle repair. Conditional deletion of TDP-43 in SCs caused a consistent and progressive loss of G<sub>Alert</sub> SCs, even in uninjured muscle, leading to depletion of the SC pool. TDP-43 haploinsufficiency was sufficient to impair SC maintenance, indicating that both alleles are required. Integrative analysis suggests that TDP-43 supports the expression of stress response-associated transcripts during the quiescent-to- G<sub>Alert</sub> transition and that failure to mount this response contributes to SC apoptosis. Thus, we identified TDP-43 as a critical regulator of survival of SCs as these cells activate, and we establish that TDP-43 is required for the maintenance and repair of skeletal muscle.</p>","PeriodicalId":21885,"journal":{"name":"Stem Cell Reports","volume":" ","pages":"103050"},"PeriodicalIF":5.6,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13555458/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148797952","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Stem Cell ReportsPub Date : 2026-09-08Epub Date: 2026-08-06DOI: 10.1016/j.stemcr.2026.103026
Hannah Rostalski, Tomi Hietanen, Dorit Hoffmann, Sami Heikkinen, Nadine Huber, Ashutosh Dhingra, Salvador Rodriguez-Nieto, Teemu Kuulasmaa, Sohvi Ohtonen, Henna Jäntti, Viivi Pekkala, Stina Leskelä, Petra Mäkinen, Kasper Katisko, Päivi Hartikainen, Šárka Lehtonen, Eino Solje, Jari Koistinaho, Tarja Malm, Anne M Portaankorva, Teemu Natunen, Henna Martiskainen, Mari Takalo, Mikko Hiltunen, Annakaisa Haapasalo
{"title":"C9orf72-associated and sporadic FTD patient iPSC-microglia show differences in phagocytosis and gene expression.","authors":"Hannah Rostalski, Tomi Hietanen, Dorit Hoffmann, Sami Heikkinen, Nadine Huber, Ashutosh Dhingra, Salvador Rodriguez-Nieto, Teemu Kuulasmaa, Sohvi Ohtonen, Henna Jäntti, Viivi Pekkala, Stina Leskelä, Petra Mäkinen, Kasper Katisko, Päivi Hartikainen, Šárka Lehtonen, Eino Solje, Jari Koistinaho, Tarja Malm, Anne M Portaankorva, Teemu Natunen, Henna Martiskainen, Mari Takalo, Mikko Hiltunen, Annakaisa Haapasalo","doi":"10.1016/j.stemcr.2026.103026","DOIUrl":"10.1016/j.stemcr.2026.103026","url":null,"abstract":"<p><p>C9orf72 hexanucleotide repeat expansion (C9-HRE) is a major genetic cause of amyotrophic lateral sclerosis and frontotemporal dementia (FTD). However, approximately half of the FTD patients are sporadic without a clear genetic background. To compare characteristics of microglia from different FTD subtypes, we generated induced pluripotent stem cell-derived microglia (iMG) from sporadic and C9-HRE-carrying behavioral variant FTD (bvFTD) patients and healthy controls. C9-HRE iMG displayed C9-HRE-associated RNA foci and dipeptide repeat proteins. All bvFTD iMG had fewer LAMP2-A-positive vesicles compared to control iMG. Additionally, C9-HRE iMG showed significantly increased LC3BII/I conversion after bafilomycin A1 treatment and altered phagocytic activity. The gene expression profile of C9-HRE iMG only modestly differed from the control iMG, but was greatly different from the sporadic bvFTD patient iMG. Our data show alterations in phagocytic and autophagosomal/lysosomal pathways and gene expression profiles between C9-HRE and sporadic bvFTD iMG for the first time.</p>","PeriodicalId":21885,"journal":{"name":"Stem Cell Reports","volume":" ","pages":"103026"},"PeriodicalIF":5.6,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13555443/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148685788","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Stem Cell ReportsPub Date : 2026-09-08Epub Date: 2026-08-06DOI: 10.1016/j.stemcr.2026.103024
Kevin P Robb, Razieh Rabani, Shabana Vohra, Shoba Singh, Jaskarndip Chahal, Julie Audet, Anthony V Perruccio, Ali Naraghi, Rajiv Gandhi, Osvaldo Espin-Garcia, Sowmya Viswanathan
{"title":"Responders vs. non-responders to mesenchymal stromal cells in knee osteoarthritis: Mechanistic correlates of donor cell and patient features.","authors":"Kevin P Robb, Razieh Rabani, Shabana Vohra, Shoba Singh, Jaskarndip Chahal, Julie Audet, Anthony V Perruccio, Ali Naraghi, Rajiv Gandhi, Osvaldo Espin-Garcia, Sowmya Viswanathan","doi":"10.1016/j.stemcr.2026.103024","DOIUrl":"10.1016/j.stemcr.2026.103024","url":null,"abstract":"<p><p>Mesenchymal stromal cell (MSC) injection has afforded heterogeneous outcomes in knee osteoarthritis (KOA). Herein, a framework that dually correlates KOA patient responsiveness with baseline autologous bone marrow-derived MSC(M) donor batch attributes and baseline clinical and biomarker features is provided. Using clinical trial data (NCT02351011), we demonstrated that MSC(M) with increased immunomodulatory potency are more efficacious. Multivariable MSC(M) genes correlated strongly with responder status and 12- and 24-month improvements in Knee Injury and Osteoarthritis Outcome Scores. Responder MSC(M) donor batches had unique microRNA expression and ability to polarize CD14<sup>+</sup> monocytes in vitro. KOA responders had lower baseline physical activity and trended toward more severe baseline KOA. Baseline local but not systemic biomarkers showed trending correlations with patient responsiveness. 42% of KOA patients were responders at 24 months, emphasizing durability of single MSC(M) injections. Together, our analytical methodology defines critical quality attributes of potent MSC(M) donor batches and identifies putative KOA patient theratypes to MSC treatments.</p>","PeriodicalId":21885,"journal":{"name":"Stem Cell Reports","volume":" ","pages":"103024"},"PeriodicalIF":5.6,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13555466/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148685829","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Stem Cell ReportsPub Date : 2026-09-08Epub Date: 2026-08-06DOI: 10.1016/j.stemcr.2026.103047
Barbara Corneo, Giovanni Faga, Inês Figueira, Jacopo Zasso, Wenli Yang, Katrin Neuman, Pia A Johansson, Lyn Healy, Laurence M Daheron, Melanie Generali, Ole Pless, Ras Trokovic, Laurent David, Mehrnaz Gazhvini, Laura Batlle-Morera
{"title":"The transformative impact of stem cell core facilities in biomedical research.","authors":"Barbara Corneo, Giovanni Faga, Inês Figueira, Jacopo Zasso, Wenli Yang, Katrin Neuman, Pia A Johansson, Lyn Healy, Laurence M Daheron, Melanie Generali, Ole Pless, Ras Trokovic, Laurent David, Mehrnaz Gazhvini, Laura Batlle-Morera","doi":"10.1016/j.stemcr.2026.103047","DOIUrl":"10.1016/j.stemcr.2026.103047","url":null,"abstract":"<p><p>Over the past three decades, advances in human pluripotent stem cell (hPSC) technologies, including induced pluripotent stem cells, gene editing, and 2D/3D models, have transformed biomedical research. These powerful tools have revolutionized disease modeling, drug discovery, and the development of advanced therapy medicinal products (ATMPs), while driving the establishment of stem cell core facilities. By providing specialized expertise, standardized workflows, and access to advanced technologies, these facilities support both fundamental and translational research, promote rigor and reproducibility, and foster collaboration. This manuscript highlights their role as hubs of excellence and discusses current challenges and future opportunities for the global stem cell community.</p>","PeriodicalId":21885,"journal":{"name":"Stem Cell Reports","volume":" ","pages":"103047"},"PeriodicalIF":5.6,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13555415/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148685756","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Stem Cell ReportsPub Date : 2026-09-08Epub Date: 2026-08-27DOI: 10.1016/j.stemcr.2026.103057
Kate E Galloway
{"title":"Luck favors the prepared in hepatic conversion.","authors":"Kate E Galloway","doi":"10.1016/j.stemcr.2026.103057","DOIUrl":"10.1016/j.stemcr.2026.103057","url":null,"abstract":"<p><p>Goto et al. in this issue use continuous lineage imaging to examine why only some fibroblasts become induced hepatocyte-like cells. The study suggests that hepatic reprogramming follows a hybrid elite-stochastic model: early asymmetric division produces elite-like lineages, and subsequent mitotic activity and chance determine which descendants ultimately complete conversion.</p>","PeriodicalId":21885,"journal":{"name":"Stem Cell Reports","volume":" ","pages":"103057"},"PeriodicalIF":5.6,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13555469/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148841135","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"A macrophage-intestinal organoid co-culture model captures balanced epithelial homeostasis and inflammation.","authors":"Lisa Tonini, Tae Baek Lee, Eunju Jang, Sungmoo Hong, Soobin Choi, Changhwan Ahn","doi":"10.1016/j.stemcr.2026.103045","DOIUrl":"10.1016/j.stemcr.2026.103045","url":null,"abstract":"<p><p>Immune-epithelial interactions are essential for intestinal homeostasis, yet organoid monocultures lack immune components and fail to model how immune cells shape epithelial identity. Here, we establish a macrophage-organoid co-culture integrating bone marrow-derived macrophages (BMDMs) into the intestinal niche to create a controlled, immune-competent system. Under homeostatic conditions, the optimized 5k configuration of BMDMs preserves crypt-like architecture and maintains stem cell localization and secretory lineage organization. TNFα stimulation induces coordinated epithelial remodeling characterized by reduced canonical stem cell marker expression and density-dependent shifts in macrophage phenotype. Transcriptomic profiling confirms enrichment of immune-associated and epithelial stress pathways. Comparative analysis with a DSS-induced murine inflammation model reveals overlapping inflammatory and epithelial remodeling features, supporting physiological relevance. This platform provides a reproducible framework for studying epithelial-immune interactions and inflammatory remodeling under defined conditions, offering a controlled alternative to animal models.</p>","PeriodicalId":21885,"journal":{"name":"Stem Cell Reports","volume":" ","pages":"103045"},"PeriodicalIF":5.6,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13555428/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148685768","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Hepatic reprogramming occurs in a time-independent manner via an initial asymmetric division and continued mitotic activity.","authors":"Nanako Goto, Shizuka Miura, Masaki Kawamata, Kenichi Horisawa, Ryoga Suzuki, Tomonori Miyata, Nao Taniguchi, Atsushi Suzuki","doi":"10.1016/j.stemcr.2026.103056","DOIUrl":"10.1016/j.stemcr.2026.103056","url":null,"abstract":"<p><p>Recent advancements in cellular reprogramming make it possible to alter cell fate, yet its mechanisms remain largely unclear. While previous studies have explored the link between cell division and reprogramming, it is still unknown why some cells reprogram under identical conditions, while others do not. In this study, we used the direct reprogramming of fibroblasts into induced hepatocyte-like cells (iHepCs) as a model to address this issue. Time-lapse imaging was performed throughout the entire reprogramming process, from the introduction of reprogramming factors to the completion of iHepC conversion. Spatiotemporal single-cell tracking revealed that the direct hepatic reprogramming follows a hybrid model, combining elite and stochastic models. Elite-like cells emerge from the earliest cell divisions, undergo random selection, and successfully reprogram a subset of their descendants. Moreover, cells that ultimately become iHepCs exhibited active division both before and after reprogramming. These results suggest that targeting active cell division may enhance reprogramming efficiency.</p>","PeriodicalId":21885,"journal":{"name":"Stem Cell Reports","volume":" ","pages":"103056"},"PeriodicalIF":5.6,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13555477/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148841140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Stem Cell ReportsPub Date : 2026-09-08Epub Date: 2026-08-20DOI: 10.1016/j.stemcr.2026.103049
Sota Nishida, Boyang An, Hayato Uchida, Shota Zenno, Takumi Nojima, Arisa Makimura, Fumihiro Morishita, Mizuki Honda, Takuya Imamura
{"title":"A human-specific non-coding RNA for EFHC1, an epilepsy-associated gene, regulates neural stem cell proliferation for cortical development.","authors":"Sota Nishida, Boyang An, Hayato Uchida, Shota Zenno, Takumi Nojima, Arisa Makimura, Fumihiro Morishita, Mizuki Honda, Takuya Imamura","doi":"10.1016/j.stemcr.2026.103049","DOIUrl":"10.1016/j.stemcr.2026.103049","url":null,"abstract":"<p><p>Epilepsy is a prevalent brain disorder in humans but rarely occurs naturally in other species, highlighting the potential for human-specific mechanisms in its pathogenesis, and thus, current animal models fail to recapitulate human symptoms. Comparing RNA sequencing (RNA-seq) datasets from human and mouse neural stem cells (NSCs), we identified EFHC1, a juvenile myoclonic epilepsy gene, as exhibiting a human-biased expression. EFHC1 knockdown reduced human NSC proliferation, while its overexpression in mouse embryonic brains increased cortical NSC number. Mechanistically, EFHC1 prevented endoplasmic reticulum stress, thereby reducing inflammatory activation of p38 MAPK and promoting continuous proliferation of human NSCs. We also identified pancEFHC1, a bidirectional promoter-associated non-coding RNA (pancRNA), located at the human EFHC1 promoter. Knockdown of pancEFHC1 in human NSCs increased DNA methylation to reduce EFHC1 expression, with the resulting phenotype rescued by EFHC1 overexpression. We propose that the evolutionary acquisition of pancEFHC1 has introduced a complex regulatory mechanism for EFHC1 expression that allows distinguishing it in humans.</p>","PeriodicalId":21885,"journal":{"name":"Stem Cell Reports","volume":" ","pages":"103049"},"PeriodicalIF":5.6,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13555433/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148797769","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Stem Cell ReportsPub Date : 2026-09-08Epub Date: 2026-08-06DOI: 10.1016/j.stemcr.2026.103027
Elena M Turkalj, Gugene Kang, Isabelle Liu, Mariami Kuljanishvili, Neda Keyhanvar, Michael C Oldham, Caroline Vissers
{"title":"Cortical organoids reveal human-specific role of METTL5 in neurodevelopment via regulation of CHCHD2.","authors":"Elena M Turkalj, Gugene Kang, Isabelle Liu, Mariami Kuljanishvili, Neda Keyhanvar, Michael C Oldham, Caroline Vissers","doi":"10.1016/j.stemcr.2026.103027","DOIUrl":"10.1016/j.stemcr.2026.103027","url":null,"abstract":"<p><p>Methyltransferase-like 5 (METTL5) catalyzes N6-methyladenosine (m<sup>6</sup>A) modification on 18S rRNA. In humans, loss-of-function mutations in METTL5 cause severe microcephaly and intellectual disability, whereas Mettl5 knockout (KO) animal models display inconsistent and milder phenotypes. To better model human disease, we generated METTL5-KO human-induced pluripotent stem cell (hiPSC)-derived cortical organoids, which exhibit impaired neural progenitor cell (NPC) proliferation and differentiation, leading to reduced ventricle-like structures and significant reductions in cortical organoid diameter. Mechanistically, Ribo-seq analysis revealed broad translational changes in METTL5-KO NPCs consistent with cellular stress responses rather than transcript-specific translational changes. Single-cell RNA-seq identified downregulation of coiled-coil-helix-coiled-coil-helix domain containing 2 (CHCHD2), a mitochondrial regulator of oxidative metabolism. Overexpression of CHCHD2 in METTL5-KO NPCs rescued proliferation and partially rescued oxidative metabolism in NPCs and ventricle formation in organoids. This highlights a previously uncharacterized connection between CHCHD2, oxidative metabolism, and METTL5-mediated regulation of human neurogenesis.</p>","PeriodicalId":21885,"journal":{"name":"Stem Cell Reports","volume":" ","pages":"103027"},"PeriodicalIF":5.6,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13555456/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148685745","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}