Pub Date : 2025-12-15DOI: 10.1016/j.matbio.2025.12.003
Valerie Horsley
This article describes the journey of my laboratory team as we became fascinated in the dynamic changes that occurred to adipose tissue in the skin during tissue injury and fibrosis. I discuss how lineage tracing and molecular manipulation of adipocyte lineage cells led us to discover novel ways that fat cells contribute to ECM homeostasis in the skin. This work revealed the importance of adipocyte plasticity and cell communication during tissue repair and as they respond to fibrotic stimuli.
{"title":"Follow the science: How fat cells taught us about scarring and ECM homeostasis","authors":"Valerie Horsley","doi":"10.1016/j.matbio.2025.12.003","DOIUrl":"https://doi.org/10.1016/j.matbio.2025.12.003","url":null,"abstract":"This article describes the journey of my laboratory team as we became fascinated in the dynamic changes that occurred to adipose tissue in the skin during tissue injury and fibrosis. I discuss how lineage tracing and molecular manipulation of adipocyte lineage cells led us to discover novel ways that fat cells contribute to ECM homeostasis in the skin. This work revealed the importance of adipocyte plasticity and cell communication during tissue repair and as they respond to fibrotic stimuli.","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"21 1","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145760382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-11DOI: 10.1016/j.matbio.2025.12.002
Maria Giulia Bigotti, Andrea Brancaccio
{"title":"α-Dystroglycan at the ECM-Cell crossroad: emerging functions of its N-terminal domain","authors":"Maria Giulia Bigotti, Andrea Brancaccio","doi":"10.1016/j.matbio.2025.12.002","DOIUrl":"https://doi.org/10.1016/j.matbio.2025.12.002","url":null,"abstract":"","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"11 1","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145732377","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-07DOI: 10.1016/j.matbio.2025.12.001
Mahdokht Mahmoodi, Claudie Berger, Mir-Hamed Nabavi, Yongjun Xiao, Lucie Canaff, Monica Pata, Jingjing Li, Mathieu Ferron, Monzur Murshed, David Goltzman, Suzanne N. Morin, Mari T. Kaartinen
{"title":"Liver-derived, circulating plasma fibronectin regulates trabecular bone mass and bone formation in adult male mice and its levels in sera associates with bone density in aging men","authors":"Mahdokht Mahmoodi, Claudie Berger, Mir-Hamed Nabavi, Yongjun Xiao, Lucie Canaff, Monica Pata, Jingjing Li, Mathieu Ferron, Monzur Murshed, David Goltzman, Suzanne N. Morin, Mari T. Kaartinen","doi":"10.1016/j.matbio.2025.12.001","DOIUrl":"https://doi.org/10.1016/j.matbio.2025.12.001","url":null,"abstract":"","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"135 1","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145689366","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Basement membranes (BM) are thin, nanoporous sheets of specialized extracellular matrix (ECM) that line epithelial tissues. They are dynamic structures that serve multiple key functions, as evidenced by numerous diseases, including cancer progression, that are associated with their alterations. Our understanding of the BM and its communication with adjoining epithelial cells remains highly fragmented due to the BM’s complex molecular architecture, the lack of molecular tools, limitations in utilizing high-resolution imaging techniques to BMs assembled on tissues, and the difficulty of assessing their functional contributions in vivo. Here, by combining multiple -omics analyses and advanced microscopy methodologies, we characterized the BM from two normal human mammary epithelial cell lines, MCF10 and HMLE, grown as spheroids in 3D matrices. Our findings indicate that the spheroids autonomously assemble a BM exhibiting all the molecular, structural, and biophysical characteristics of physiological BM. Using these minimalist model systems, we provide evidence that collagen IV, laminins, perlecan, and hemidesmosomes all overlap in a shared porous lattice. Next, we demonstrate that the invasion-promoting PSD4/EFA6B knockout, found in patients with breast cancer, decreases the expression of BM components and their assembly on the spheroid surface. We then show that invasive spheroids develop enlarged pores in the BM via filopodia-like plasma membrane extensions, which further expand in a protease-dependent manner, thereby facilitating the passage of invasive cells.
{"title":"Human mammary 3D spheroid models uncover the role of filopodia in breaching the basement membrane to facilitate invasion","authors":"Alain Corinus , Sophie Abélanet , Julia Dubreuil , Zhenyu Zhu , Sabrina Pisano , Christelle Boscagli , Anne-Sophie Gay , Delphine Debayle , Marin Truchi , Kevin Lebrigand , Sandra Lacas-Gervais , Frédéric Brau , Xavier Descombes , Patricia Rousselle , Michel Franco , Frédéric Luton","doi":"10.1016/j.matbio.2025.11.008","DOIUrl":"10.1016/j.matbio.2025.11.008","url":null,"abstract":"<div><div>Basement membranes (BM) are thin, nanoporous sheets of specialized extracellular matrix (ECM) that line epithelial tissues. They are dynamic structures that serve multiple key functions, as evidenced by numerous diseases, including cancer progression, that are associated with their alterations. Our understanding of the BM and its communication with adjoining epithelial cells remains highly fragmented due to the BM’s complex molecular architecture, the lack of molecular tools, limitations in utilizing high-resolution imaging techniques to BMs assembled on tissues, and the difficulty of assessing their functional contributions <em>in vivo</em>. Here, by combining multiple -omics analyses and advanced microscopy methodologies, we characterized the BM from two normal human mammary epithelial cell lines, MCF10 and HMLE, grown as spheroids in 3D matrices. Our findings indicate that the spheroids autonomously assemble a BM exhibiting all the molecular, structural, and biophysical characteristics of physiological BM. Using these minimalist model systems, we provide evidence that collagen IV, laminins, perlecan, and hemidesmosomes all overlap in a shared porous lattice. Next, we demonstrate that the invasion-promoting <em>PSD4</em>/EFA6B knockout, found in patients with breast cancer, decreases the expression of BM components and their assembly on the spheroid surface. We then show that invasive spheroids develop enlarged pores in the BM via filopodia-like plasma membrane extensions, which further expand in a protease-dependent manner, thereby facilitating the passage of invasive cells.</div></div>","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"143 ","pages":"Pages 36-47"},"PeriodicalIF":4.8,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145657542","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-26DOI: 10.1016/j.matbio.2025.11.007
Andrew Leask
The matricellular protein CCN1 is pro-senescent, and can be considered as a possible inducer of the senescence-associated secretory phenotype (SASP). Although the SASP facilitates healthy tissue repair when senescent cells are properly cleared, pathological fibrosis results when this clearance is defective. Similarly, CCN1 can have both anti-fibrotic and pro-fibrotic properties, depending on the context. Recent data indicate that although CCN1 has anti-fibrotic roles in normal tissue repair and the liver, it also has pro-fibrotic roles in lung, kidney, cardiac, skin and liver fibrosis/scarring. That CCN1 has context-dependent roles in fibrosis deserves consideration when developing anti-fibrotic drugs.
{"title":"CCN1: a SASPy protein that plays multifaceted roles in fibrogenesis","authors":"Andrew Leask","doi":"10.1016/j.matbio.2025.11.007","DOIUrl":"10.1016/j.matbio.2025.11.007","url":null,"abstract":"<div><div>The matricellular protein CCN1 is pro-senescent, and can be considered as a possible inducer of the senescence-associated secretory phenotype (SASP). Although the SASP facilitates healthy tissue repair when senescent cells are properly cleared, pathological fibrosis results when this clearance is defective. Similarly, CCN1 can have both anti-fibrotic and pro-fibrotic properties, depending on the context. Recent data indicate that although CCN1 has anti-fibrotic roles in normal tissue repair and the liver, it also has pro-fibrotic roles in lung, kidney, cardiac, skin and liver fibrosis/scarring. That CCN1 has context-dependent roles in fibrosis deserves consideration when developing anti-fibrotic drugs.</div></div>","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"143 ","pages":"14"},"PeriodicalIF":4.8,"publicationDate":"2025-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145598946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-19DOI: 10.1016/j.matbio.2025.11.006
Tolg C , Price M , Leith S , Miller T , Pavanel H , A.C. Nelson , Hill KA , McCarthy JB , Turley EA
Hyaluronan (HA) metabolism in prostate cancer associates with androgen resistance and metastasis. We showed that binding of low molecular weight HA (≤250 kDa) to castration-resistant prostate cancer cells was heterogeneous with most cells binding low amounts of HA (HAlow) while a minor subset bound higher amounts of this polysaccharide (HAhigh). HAhigh subsets, which were separated by FACS, were stably more metastatic in vivo than HAlow comparators. Multiplexed flow cytometry analyses indicated that both subsets displayed similar expression of the HA receptor CD44 while an elevated RHAMM cell surface display was unique to HAhigh subsets. Genomic deletion of RHAMM using CRISPR-Cas9 editing reduced the detection of HAhigh subsets by 6mer but not 250 kDa HA fluorescent probes, and phenocopied the lower aggressive properties of HAlow tumor cells. Few differences in the mutation landscape of RHAMM+/+ vs. RHAMM-/- tumor cells were detected but pathway analyses of differentially expressed genes predicted RHAMM-loss altered extracellular matrix signaling. Transcriptomic analyses revealed that HAhigh subsets and RHAMM+/+ PC3MLN4 cells shared high expression of follistatin (FST), an activin member of the TGF-β family that is clinically linked to metastases in PCA patients. A causal role for FST in RHAMM+/+ tumor cell aggression was assessed using motility as a surrogate marker of invasive capability. FST antibodies blocked RHAMM+/+ PC3MLN4 cell migration while conversely, recombinant FST protein rescued the migration deficit of RHAMM-/- comparators. These results define a novel form of prostate cancer cell heterogeneity, identify a method for detecting and isolating highly metastatic subsets and highlight a novel RHAMM-regulated pathway that may be targeted to improve patient management by limiting metastasis.
{"title":"High hyaluronan binding and RHAMM expression identify an invasive and metastatic subpopulation in androgen-resistant prostate cancer cells","authors":"Tolg C , Price M , Leith S , Miller T , Pavanel H , A.C. Nelson , Hill KA , McCarthy JB , Turley EA","doi":"10.1016/j.matbio.2025.11.006","DOIUrl":"10.1016/j.matbio.2025.11.006","url":null,"abstract":"<div><div>Hyaluronan (HA) metabolism in prostate cancer associates with androgen resistance and metastasis. We showed that binding of low molecular weight HA (≤250 kDa) to castration-resistant prostate cancer cells was heterogeneous with most cells binding low amounts of HA (HA<sup>low</sup>) while a minor subset bound higher amounts of this polysaccharide (HA<sup>high</sup>). HA<sup>high</sup> subsets, which were separated by FACS, were stably more metastatic in vivo than HA<sup>low</sup> comparators. Multiplexed flow cytometry analyses indicated that both subsets displayed similar expression of the HA receptor CD44 while an elevated RHAMM cell surface display was unique to HA<sup>high</sup> subsets. Genomic deletion of <em>RHAMM</em> using CRISPR-Cas9 editing reduced the detection of HA<sup>high</sup> subsets by 6mer but not 250 kDa HA fluorescent probes, and phenocopied the lower aggressive properties of HA<sup>low</sup> tumor cells. Few differences in the mutation landscape of <em>RHAMM</em><sup>+/+</sup> vs. <em>RHAMM</em><sup>-/-</sup> tumor cells were detected but pathway analyses of differentially expressed genes predicted <em>RHAMM</em>-loss altered extracellular matrix signaling. Transcriptomic analyses revealed that HA<sup>high</sup> subsets and <em>RHAMM<sup>+</sup></em><sup>/+</sup> PC3MLN4 cells shared high expression of follistatin (FST), an activin member of the TGF-β family that is clinically linked to metastases in PCA patients. A causal role for FST in <em>RHAMM</em><sup>+/+</sup> tumor cell aggression was assessed using motility as a surrogate marker of invasive capability. FST antibodies blocked <em>RHAMM</em><sup>+/+</sup> PC3MLN4 cell migration while conversely, recombinant FST protein rescued the migration deficit of <em>RHAMM</em><sup>-/-</sup> comparators. These results define a novel form of prostate cancer cell heterogeneity, identify a method for detecting and isolating highly metastatic subsets and highlight a novel RHAMM-regulated pathway that may be targeted to improve patient management by limiting metastasis.</div></div>","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"143 ","pages":"Pages 23-35"},"PeriodicalIF":4.8,"publicationDate":"2025-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145559902","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-15DOI: 10.1016/j.matbio.2025.11.003
Arthur Lauri Pasanen-Zentz , Mengjie Zhu , Sebastian Schmitz , Nitin George Eapen , Matthias Pzryklenk , Fabian Metzen , Karina Hadrian , Matthias Mörgelin , Uwe Hansen , Branko Zevnik , Simon E Tröder , Felix Bock , Catherine Moali , Marcus Krüger , Manuel Koch , Mats Paulsson , Raimund Wagener , Alvise Schiavinato
Collagen VI is a heterotrimeric, ubiquitously expressed microfibrillar collagen with a complex intracellular and extracellular assembly process. In addition to a short collagenous region, it is primarily composed of von Willebrand factor A (VWA) domains. Notably, only the C-terminal end of the α3 chain contains other domain types, including a Kunitz-like C5 domain, which has been reported to be necessary for microfibril formation, to function as a matrikine and exhibit biomarker properties. This region of the α3 chain undergoes proteolytic processing, with cleavage sites identified for proprotein convertases, matrix metalloproteinases (MMPs), and bone morphogenetic protein 1 (BMP1). Cleavage by furin-like convertases results in the generation of a mature collagen VI α3 chain lacking its 70 kDa C2-C5 domains. Here, we provide the first characterization of the functional significance of the furin-like cleavage site, demonstrating that while it is constitutively used, it is not essential for collagen VI assembly, microfibril formation, or skeletal muscle function under physiological conditions, likely due to the presence of redundant cleavage sites. We also present an initial characterization of the biological activity of the released fragments on myoblast cultures showing that they do not affect C2C12 myoblast behaviour or differentiation. These findings deepen our understanding of α3 chain processing and highlight its potential significance for collagen VI assembly and function, including the generation of peptides with potential biomarker and biological activity properties.
{"title":"Furin-like cleavage at the C1-C2 linker region of the ⍺3 chain is not required for collagen VI assembly","authors":"Arthur Lauri Pasanen-Zentz , Mengjie Zhu , Sebastian Schmitz , Nitin George Eapen , Matthias Pzryklenk , Fabian Metzen , Karina Hadrian , Matthias Mörgelin , Uwe Hansen , Branko Zevnik , Simon E Tröder , Felix Bock , Catherine Moali , Marcus Krüger , Manuel Koch , Mats Paulsson , Raimund Wagener , Alvise Schiavinato","doi":"10.1016/j.matbio.2025.11.003","DOIUrl":"10.1016/j.matbio.2025.11.003","url":null,"abstract":"<div><div>Collagen VI is a heterotrimeric, ubiquitously expressed microfibrillar collagen with a complex intracellular and extracellular assembly process. In addition to a short collagenous region, it is primarily composed of von Willebrand factor A (VWA) domains. Notably, only the C-terminal end of the α3 chain contains other domain types, including a Kunitz-like C5 domain, which has been reported to be necessary for microfibril formation, to function as a matrikine and exhibit biomarker properties. This region of the α3 chain undergoes proteolytic processing, with cleavage sites identified for proprotein convertases, matrix metalloproteinases (MMPs), and bone morphogenetic protein 1 (BMP1). Cleavage by furin-like convertases results in the generation of a mature collagen VI α3 chain lacking its 70 kDa C2-C5 domains. Here, we provide the first characterization of the functional significance of the furin-like cleavage site, demonstrating that while it is constitutively used, it is not essential for collagen VI assembly, microfibril formation, or skeletal muscle function under physiological conditions, likely due to the presence of redundant cleavage sites. We also present an initial characterization of the biological activity of the released fragments on myoblast cultures showing that they do not affect C2C12 myoblast behaviour or differentiation. These findings deepen our understanding of α3 chain processing and highlight its potential significance for collagen VI assembly and function, including the generation of peptides with potential biomarker and biological activity properties.</div></div>","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"143 ","pages":"Pages 1-13"},"PeriodicalIF":4.8,"publicationDate":"2025-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145531347","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-15DOI: 10.1016/j.matbio.2025.11.004
Graziamaria Paradisi, Valeria Bonavolontà, Martina Venditti, Giulia Fasano, Catia Pedalino, Filippo Del Bene, Marco Tartaglia, Antonella Lauri
Pathogenic variants in COL4A1 and COL4A2, encoding type IV collagen α1 and α2 chains—core components of all basement membranes—cause a multisystem disorder with variable expressivity. Affected individuals commonly present with cerebral small vessel disease (cSVD), unmanageable intracerebral haemorrhage (ICH), drug-resistant epilepsy, microphthalmia, and congenital cataract. Severe phenotypes are often linked to glycine substitutions that disrupt α1/α2 heterotrimer assembly, though insertions, deletions, and haploinsufficiency seem to also be pathogenic. Limited insight into collagen IV α1 and α2 biology and how specific variants affect their functions—coupled with a lack of rapid in vivo assays for functional variants classification—hampers patient stratification and therapy development. Here, we established and characterized two complementary col4a1 knockdown (KD) models in zebrafish. Taking advantages of their transparency and rapid development we set-up in vivo assays for neurovascular and ocular phenotyping. Both models reproduced key features of human disease, including ventriculomegaly, vascular fragility with spontaneous and trauma-induced ICH, microphthalmia, and cataracts. Notably, expression of human wild-type COL4A1 partially rescued most of the observed defects, while pathogenic glycine-substitution variants failed to do so. These findings validate col4a1 KD in zebrafish as a robust in vivo model of some aspects of COL4A1/A2 syndrome, highlighting a conserved role of collagen IV α1 in neurovascular and ocular development. Our results also support haploinsufficiency as a contributing pathogenic mechanism, alongside dominant-negative effects. This work lays the foundation for the use of zebrafish to support rapid COL4A1 and COL4A2 variants pathogenicity assessment and mechanistic studies, with the potential to accelerate development of targeted therapies.
{"title":"Zebrafish col4a1 loss-of-function models mirror key neurovascular and ocular features of COL4A1/A2 syndrome and enable human variants assessment in vivo","authors":"Graziamaria Paradisi, Valeria Bonavolontà, Martina Venditti, Giulia Fasano, Catia Pedalino, Filippo Del Bene, Marco Tartaglia, Antonella Lauri","doi":"10.1016/j.matbio.2025.11.004","DOIUrl":"https://doi.org/10.1016/j.matbio.2025.11.004","url":null,"abstract":"Pathogenic variants in <ce:italic>COL4A1</ce:italic> and <ce:italic>COL4A2</ce:italic>, encoding type IV collagen α1 and α2 chains—core components of all basement membranes—cause a multisystem disorder with variable expressivity. Affected individuals commonly present with cerebral small vessel disease (cSVD), unmanageable intracerebral haemorrhage (ICH), drug-resistant epilepsy, microphthalmia, and congenital cataract. Severe phenotypes are often linked to glycine substitutions that disrupt α1/α2 heterotrimer assembly, though insertions, deletions, and haploinsufficiency seem to also be pathogenic. Limited insight into collagen IV α1 and α2 biology and how specific variants affect their functions—coupled with a lack of rapid <ce:italic>in vivo</ce:italic> assays for functional variants classification—hampers patient stratification and therapy development. Here, we established and characterized two complementary <ce:italic>col4a1</ce:italic> knockdown (KD) models in zebrafish. Taking advantages of their transparency and rapid development we set-up <ce:italic>in vivo</ce:italic> assays for neurovascular and ocular phenotyping. Both models reproduced key features of human disease, including ventriculomegaly, vascular fragility with spontaneous and trauma-induced ICH, microphthalmia, and cataracts. Notably, expression of human wild-type COL4A1 partially rescued most of the observed defects, while pathogenic glycine-substitution variants failed to do so. These findings validate <ce:italic>col4a1</ce:italic> KD in zebrafish as a robust <ce:italic>in vivo</ce:italic> model of some aspects of COL4A1/A2 syndrome, highlighting a conserved role of collagen IV α1 in neurovascular and ocular development. Our results also support haploinsufficiency as a contributing pathogenic mechanism, alongside dominant-negative effects. This work lays the foundation for the use of zebrafish to support rapid <ce:italic>COL4A1</ce:italic> and <ce:italic>COL4A2</ce:italic> variants pathogenicity assessment and mechanistic studies, with the potential to accelerate development of targeted therapies.","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"120 1","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145531352","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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