Disease Models & Mechanisms最新文献

Human induced pluripotent stem cell-derived inner ear organoids reveal hair cell damage and plasticity after cisplatin and gentamicin exposure. 顺铂和庆大霉素暴露后，人诱导多能干细胞衍生的内耳类器官显示毛细胞损伤和可塑性。

IF 3.3 3区医学

Disease Models & Mechanisms Pub Date : 2026-06-01 Epub Date: 2026-03-03 DOI: 10.1242/dmm.052511

Amy W A Lucassen, Winnie M C van den Boogaard, Esther Fousert, Jingyuan Zhang, Karl R Koehler, John C M J de Groot, Peter Paul G van Benthem, Wouter H van der Valk, Heiko Locher

{"title":"Human induced pluripotent stem cell-derived inner ear organoids reveal hair cell damage and plasticity after cisplatin and gentamicin exposure.","authors":"Amy W A Lucassen, Winnie M C van den Boogaard, Esther Fousert, Jingyuan Zhang, Karl R Koehler, John C M J de Groot, Peter Paul G van Benthem, Wouter H van der Valk, Heiko Locher","doi":"10.1242/dmm.052511","DOIUrl":"10.1242/dmm.052511","url":null,"abstract":"Ototoxicity is a leading cause of sensory deficits, including hearing loss and balance disorders. Predicting ototoxicity is challenging owing to translatability issues of animal models and limited access to human inner ear tissue. Known ototoxic drugs, such as cisplatin (a chemotherapeutic) and gentamicin (an aminoglycoside antibiotic), cause irreversible damage to sensory hair cells and neurons. Here, we establish human induced pluripotent stem cell (hiPSC)-derived inner ear organoids as an in vitro model for studying ototoxicity. Exposure to cisplatin and gentamicin led to hair cell and neuronal loss, disrupted organoid architecture and increased cell damage, including apoptosis, in a dose-dependent manner. Remarkably, prolonged culture of treated organoids showed re-emergence of otic vesicle structures with sensory hair cells and neurons. SOX10+ otic epithelial cells exhibited increased Ki-67 expression, indicating a potential for developmental plasticity. Our findings demonstrate the value of hiPSC-derived inner ear organoids as a platform for human ototoxicity modeling and provide a basis for testing otoprotective interventions, offering insights into the intrinsic plasticity of developing inner ear cells.","PeriodicalId":11144,"journal":{"name":"Disease Models & Mechanisms","volume":"19 6","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12994450/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147343806","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A 3D lymph node model for chronic lymphocytic leukaemia recapitulates microenvironmental features and drug response in vitro. 慢性淋巴细胞白血病的三维淋巴结模型概括了体外微环境特征和药物反应。

IF 3.3 3区医学

Disease Models & Mechanisms Pub Date : 2026-06-01 Epub Date: 2026-03-31 DOI: 10.1242/dmm.052731

Daniela Belloni, Dafne Barozzi, Giulia Milani, Federica Barbaglio, Aswin Raj Puthukkunnath, Pamela Ranghetti, Eleonora Perotta, Teresa Musco, Marta Sampietro, Maurilio Ponzoni, Lydia Scarfò, Paolo Ghia, Cristina Scielzo

{"title":"A 3D lymph node model for chronic lymphocytic leukaemia recapitulates microenvironmental features and drug response in vitro.","authors":"Daniela Belloni, Dafne Barozzi, Giulia Milani, Federica Barbaglio, Aswin Raj Puthukkunnath, Pamela Ranghetti, Eleonora Perotta, Teresa Musco, Marta Sampietro, Maurilio Ponzoni, Lydia Scarfò, Paolo Ghia, Cristina Scielzo","doi":"10.1242/dmm.052731","DOIUrl":"10.1242/dmm.052731","url":null,"abstract":"Chronic lymphocytic leukaemia (CLL) cells circulate between the blood, bone marrow (BM) and lymphoid organs, where interactions with the lymph node (LN) microenvironment enhance their survival, proliferation and drug resistance. Most in vitro models fail to reproduce the spatial and cellular complexity of the LN niche, limiting studies of tissue-specific drug responses. To address this, we developed a 3D LN model using a gelatine scaffold and a clinorotator bioreactor previously validated for a BM system. The scaffold was seeded with human lymphatic fibroblasts and endothelial cells, which deposited extracellular matrix and supported patient-derived CLL cell viability and proliferation. Consistent with in vivo observations, CLL cells within the scaffold downregulated the chemokine receptor CXCR4, further reduced upon proliferative stimulation. Final validation involved treatment with targeted therapies: the BCL-2 antagonist venetoclax and the BTK inhibitor ibrutinib. Venetoclax treatment revealed greater CLL protection within the LN environment than in BM, whereas the mobilizing effect of ibrutinib was comparable between these two niches. This 3D LN model offers an effective ex vivo platform for studying microenvironment-tumour interactions and tissue-specific drug responses.","PeriodicalId":11144,"journal":{"name":"Disease Models & Mechanisms","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13072081/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146124026","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Gut instinct drives discovery: an interview with Hans Clevers. 直觉驱动发现：对汉斯·克莱弗斯的采访。

IF 3.3 3区医学

Disease Models & Mechanisms Pub Date : 2026-06-01 Epub Date: 2026-03-19 DOI: 10.1242/dmm.052860

Hans Clevers

引用次数: 0

Compound design of a patient-derived 3D cell culture system modelling early peritoneal endometriosis. 模拟早期腹膜子宫内膜异位症患者来源的三维细胞培养系统的复合设计。

IF 3.3 3区医学

Disease Models & Mechanisms Pub Date : 2026-06-01 Epub Date: 2026-02-02 DOI: 10.1242/dmm.052436

Muhammad D R Rahmana, Christopher J Hill, Bettina Wilm, Dharani K Hapangama

{"title":"Compound design of a patient-derived 3D cell culture system modelling early peritoneal endometriosis.","authors":"Muhammad D R Rahmana, Christopher J Hill, Bettina Wilm, Dharani K Hapangama","doi":"10.1242/dmm.052436","DOIUrl":"10.1242/dmm.052436","url":null,"abstract":"Peritoneal endometriosis causes pelvic pain and infertility, but the underlying mechanisms related to these symptoms are not fully understood. Endometriosis diagnosis is typically delayed; thus, patient samples are unsuitable to study early endometriosis formation in situ. We generated a 3D co-culture model of early peritoneal endometriosis using patient-derived primary cells, providing unique opportunities to examine endometriotic lesion initiation and progression. The successful assembly of a simple peritoneum layer model comprising a mesothelial monolayer, basement membrane and underlying fibroblasts was achieved by embedding human peritoneal fibroblasts in a Matrigel-collagen I matrix and subsequent seeding with a layer of donor-matched human peritoneal mesothelial cells, while secretion of tissue plasminogen activator demonstrated functional mesothelial physiology. Endometrial epithelial organoids were co-cultured with endometrial stromal cells to form endometrial assembloids mimicking shed endometrial tissue fragments at menstruation, which adhered onto the peritoneal layer model, simulating early endometriotic lesion formation. Our modifiable superficial endometriosis model allows for further refinement to determine the underlying molecular mechanism(s) involved in endometriotic lesion formation.","PeriodicalId":11144,"journal":{"name":"Disease Models & Mechanisms","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12919959/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145755565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

C. elegans models of alternating hemiplegia of childhood have dominant neuromuscular junction defects. 秀丽隐杆线虫模型的儿童交替偏瘫有主要的神经肌肉连接缺陷。

IF 3.3 3区医学

Disease Models & Mechanisms Pub Date : 2026-05-01 DOI: 10.1242/dmm.052809

Diana A Wall, Adam M Friedberg, Jeremy Lins, Roza Khalifa, Sienna Partipillo, Anne C Hart

{"title":"C. elegans models of alternating hemiplegia of childhood have dominant neuromuscular junction defects.","authors":"Diana A Wall, Adam M Friedberg, Jeremy Lins, Roza Khalifa, Sienna Partipillo, Anne C Hart","doi":"10.1242/dmm.052809","DOIUrl":"10.1242/dmm.052809","url":null,"abstract":"Dominant missense mutations in ATP1A3, encoding a Na+, K+ ATPase α-3 subunit, can cause Alternating Hemiplegia of Childhood (AHC), but how these mutations lead to AHC remains unclear. Here, we establish the first C. elegans AHC models by introducing AHC-causing ATP1A3 patient mutations (D801N, E815K, L839P, and G947R) into the orthologous gene, eat-6, using CRISPR/Cas9. Homozygous C. elegans AHC model animals have recessive developmental defects. Heterozygous AHC model animals have dominant defects in neuromuscular junction (NMJ) function that are inconsistent with haploinsufficiency and dominant sleep or arousal defects. Previous work in a Drosophila G755S AHC model found that loss of a K⁺-dependent, Na⁺/Ca²⁺ exchanger exacerbated neuronal defects. We introduced a loss-of-function allele of the orthologous C. elegans gene, ncx-4, into C. elegans AHC models; loss of ncx-4 function did not consistently alter C. elegans AHC model defects across alleles. Our results establish novel C. elegans models of AHC with robust phenotypes, demonstrate that AHC mutations disrupt NMJ function, and provide proof-of-concept for discovering cross-species modifiers of AHC-related phenotypes.","PeriodicalId":11144,"journal":{"name":"Disease Models & Mechanisms","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Myeloperoxidase impairs mucociliary transport on human airway epithelium. 髓过氧化物酶损害人气道上皮粘膜纤毛运输。

IF 3.3 3区医学

Disease Models & Mechanisms Pub Date : 2026-05-01 DOI: 10.1242/dmm.052764

Allison Boboltz, Vaidehi Rathi, Sahana Kumar, Gregg A Duncan

{"title":"Myeloperoxidase impairs mucociliary transport on human airway epithelium.","authors":"Allison Boboltz, Vaidehi Rathi, Sahana Kumar, Gregg A Duncan","doi":"10.1242/dmm.052764","DOIUrl":"10.1242/dmm.052764","url":null,"abstract":"Dampening neutrophil-driven inflammation in the airways remains a challenge in treating cystic fibrosis (CF) lung disease. Myeloperoxidase (MPO) is a neutrophilic enzyme that produces reactive oxygen species and is highly concentrated in CF airways. Greater MPO concentrations have been previously correlated with increased mucus plugging in bronchiectasis, suggesting that MPO could impair mucociliary transport. As such, we evaluated the impact of MPO treatment on barrier integrity, mucin production, mucus viscoelasticity, and mucociliary transport in fully differentiated human airway epithelial cultures at ionic conditions reflective of the healthy and CF-affected airways. Using live cell imaging and particle velocimetry, we found that MPO inhibits mucociliary transport in vitro at CF-like and normal airway conditions. The impairment of mucus clearance by MPO was similar to neutrophil elastase (NE), another neutrophilic granular enzyme that damages the host tissues and impairs airway clearance. We also found subsequent treatment with the reducing agent, N-acetyl cysteine, could alleviate MPO-mediated mucociliary dysfunction through disulfide bond cleavage. These findings identify MPO as a therapeutic target to resolve deficits in airway clearance function in CF and related muco-obstructive lung diseases.","PeriodicalId":11144,"journal":{"name":"Disease Models & Mechanisms","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Evaluating skeletal muscle dysfunction and recovery in a zymosan model of critical illness in mice. 评估骨骼肌功能障碍和恢复的酶酶酶模型的危重疾病的小鼠。

IF 3.3 3区医学

Disease Models & Mechanisms Pub Date : 2026-04-24 DOI: 10.1242/dmm.052712

Amy J Bongetti, Annabel Chee, John H V Nguyen, Jin D Chung, Wenlan Li, Kristy Swiderski, Yasmine Ali Abdelhamid, Olav E Rooyackers, Marissa K Caldow, Gordon S Lynch

{"title":"Evaluating skeletal muscle dysfunction and recovery in a zymosan model of critical illness in mice.","authors":"Amy J Bongetti, Annabel Chee, John H V Nguyen, Jin D Chung, Wenlan Li, Kristy Swiderski, Yasmine Ali Abdelhamid, Olav E Rooyackers, Marissa K Caldow, Gordon S Lynch","doi":"10.1242/dmm.052712","DOIUrl":"https://doi.org/10.1242/dmm.052712","url":null,"abstract":"Muscle wasting and weakness are common complications associated with critical illness and admission to the Intensive Care Unit (ICU), that contribute to increased mortality and health deficits post-discharge. The mechanisms underlying ICU-acquired muscle weakness (ICU-AW) are incompletely understood and small animal models can help address this shortfall and provide experimental platforms for devising therapeutic strategies. We used a zymosan model to induce wasting, and weakness in C57BL/6J mice and evaluated recovery of hindlimb muscles and diaphragm at 4, 7, 14, and 28 days (D) after induction of critical illness, through extensive physiological and immunohistological analyses. Tibialis anterior (TA) muscles from zymosan treated mice exhibited atrophy and functional impairment at D4 and D7 with recovery at D14. In contrast, the DIA exhibited a delay in wasting and recovery from critical illness, with muscle fibre atrophy at D28 despite inflammatory cell infiltration from D4 and transient impairments in respiratory function. The zymosan mouse model provides important insights into mechanisms underlying the recovery from wasting and weakness after critical illness to better understand and treat ICU-AW.","PeriodicalId":11144,"journal":{"name":"Disease Models & Mechanisms","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147765326","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Dolutegravir developmental toxicity is mitigated by magnesium and folate in zebrafish embryos. 镁和叶酸在斑马鱼胚胎中减轻了多替格拉韦的发育毒性。

IF 3.3 3区医学

Disease Models & Mechanisms Pub Date : 2026-04-23 DOI: 10.1242/dmm.052632

Robert M Cabrera, Ahmed Mohamed, Ryoko Minowa, Katheryn A Neugebauer, Daniel A Gorelick

{"title":"Dolutegravir developmental toxicity is mitigated by magnesium and folate in zebrafish embryos.","authors":"Robert M Cabrera, Ahmed Mohamed, Ryoko Minowa, Katheryn A Neugebauer, Daniel A Gorelick","doi":"10.1242/dmm.052632","DOIUrl":"https://doi.org/10.1242/dmm.052632","url":null,"abstract":"Integrase strand transfer inhibitors have transformed HIV therapy, yet the widely prescribed drug dolutegravir (DTG) has been linked to developmental toxicity and its teratogenic mechanism remains unclear. Here we use zebrafish to dissect DTG toxicity during early vertebrate development. DTG exposure from 2-4 hours post-fertilization (hpf) to 24 hpf produced high mortality and abnormal morphology. Co-treatment with folates partially restored normal morphology, whereas calcium had no effect. Strikingly, supplementation with magnesium (Mg) partially rescued DTG-exposed embryos, implicating magnesium availability in protection. In competitive binding assays, Mg increased binding of folate to purified folate receptor (FOLR1) by 30% in the presence of DTG. folr1 mutant embryos contained significantly less endogenous folate than wild-type embryos and displayed marked hypersensitivity to DTG that could not be mitigated by folate supplementation. Critically, magnesium supplementation partially rescued DTG toxicity in folr1 mutants, indicating a Folr1-independent component and placing the balance between free DTG and Mg-bound DTG upstream of folate transport. These results support a model in which free DTG antagonizes FOLR1 and Mg modifies DTG developmental toxicity through both FOLR1-dependent and independent processes.","PeriodicalId":11144,"journal":{"name":"Disease Models & Mechanisms","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147765342","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Distinct cellular effects of myotonic dystrophy type 2 RAN tetrapeptides in Drosophila melanogaster. 肌强直性营养不良2型RAN四肽对黑腹果蝇的不同细胞效应。

IF 3.3 3区医学

Disease Models & Mechanisms Pub Date : 2026-04-20 DOI: 10.1242/dmm.052729

Marta Marzullo, Assia De Simone, Marta Terribili, Michela Di Salvio, Degisew Yinur Mengistu, Maria Patrizia Somma, Rodrigo D'Amico, Gianluca Canettieri, Gianluca Cestra, Laura Ciapponi

{"title":"Distinct cellular effects of myotonic dystrophy type 2 RAN tetrapeptides in Drosophila melanogaster.","authors":"Marta Marzullo, Assia De Simone, Marta Terribili, Michela Di Salvio, Degisew Yinur Mengistu, Maria Patrizia Somma, Rodrigo D'Amico, Gianluca Canettieri, Gianluca Cestra, Laura Ciapponi","doi":"10.1242/dmm.052729","DOIUrl":"https://doi.org/10.1242/dmm.052729","url":null,"abstract":"Myotonic dystrophy type 2 (DM2) is an autosomal dominant, multisystemic disorder caused by the expansion of CCTG repeats in the first intron of the CNBP gene. Repeat-associated non-AUG (RAN) translation of the expanded CCTG RNA generates two tetrapeptide repeat proteins (TPRs), polyQAGR and polyLPAC, whose roles in DM2 pathogenesis remain unclear. To define their individual contributions, we expressed codon-optimized polyQAGR and polyLPAC peptides with an ATG start codon in Drosophila melanogaster. Expression of both TPRs reduced viability and lifespan and induced eye degeneration and locomotor defects. We found that polyQAGR accumulated in the nucleolus, disrupted nucleolar integrity, and impaired rRNA processing. It also interfered with autophagy, promoting Atg5 and Atg7 transcription and accumulation of Atg8a- and Ref(2)P-positive aggregates. Consistently, overexpression of Atg8a or Ref(2)P mitigated polyQAGR-induced eye toxicity, whereas knockdown of autophagy genes worsened it. Conversely, polyLPAC increase the cytoplasmic pool of TIAR in human cells and in DM2 patient-derived myoblasts. Together, these findings show that polyQAGR and polyLPAC exert distinct toxic effects that likely converge to drive DM2 pathogenesis and may represent promising therapeutic targets.","PeriodicalId":11144,"journal":{"name":"Disease Models & Mechanisms","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147722024","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Transgenic mouse models for investigating human DUX4 expression during development and its roles in FSHD pathophysiology. 用于研究人类发育过程中DUX4表达及其在FSHD病理生理中的作用的转基因小鼠模型。

IF 3.3 3区医学

Disease Models & Mechanisms Pub Date : 2026-04-07 DOI: 10.1242/dmm.052637

Yosuke Hiramuki, Charis L Himeda, Peter L Jones, Takako I Jones

{"title":"Transgenic mouse models for investigating human DUX4 expression during development and its roles in FSHD pathophysiology.","authors":"Yosuke Hiramuki, Charis L Himeda, Peter L Jones, Takako I Jones","doi":"10.1242/dmm.052637","DOIUrl":"10.1242/dmm.052637","url":null,"abstract":"Facioscapulohumeral muscular dystrophy (FSHD) is an autosomal dominant myopathy caused by aberrant expression of the DUX4 retrogene, and it affects skeletal muscles primarily in the face, shoulder, and limbs. In healthy individuals, DUX4 is expressed in early development and is subsequently silenced in most somatic tissues. The spatiotemporal pattern of DUX4 mis-expression beyond the cleavage stage in FSHD is poorly understood because DUX4 is not well conserved beyond primates. Here, we generated Cre reporter mouse lines with human DUX4 regulatory elements to investigate the cell lineages derived from DUX4-expressing cells in embryos and adults. Intriguingly, we found that DUX4-expressing cell lineages were present in embryonic forelimb, hindlimb, and face. In adults, the reporter was expressed strongly in testis and to a lesser extent in other tissues, including weak, sporadic expression in skeletal muscles, reminiscent of mosaic DUX4 expression in FSHD. Within skeletal muscles, DUX4 lineage cells include pericytes, an interstitial cell that contributes to muscle regeneration and repair. Overall, this study introduces a new research tool for the field, and provides new insight into potential developmental mechanisms underlying FSHD pathophysiology.","PeriodicalId":11144,"journal":{"name":"Disease Models & Mechanisms","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147627422","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0