Alejandro E Mayorca-Guiliani, Diana Julie Leeming, Kim Henriksen, Joachim Høg Mortensen, Signe Holm Nielsen, Quentin M Anstee, Arun J Sanyal, Morten A Karsdal, Detlef Schuppan
{"title":"ECM formation and degradation during fibrosis, repair, and regeneration.","authors":"Alejandro E Mayorca-Guiliani, Diana Julie Leeming, Kim Henriksen, Joachim Høg Mortensen, Signe Holm Nielsen, Quentin M Anstee, Arun J Sanyal, Morten A Karsdal, Detlef Schuppan","doi":"10.1038/s44324-025-00063-4","DOIUrl":null,"url":null,"abstract":"<p><p>Imperfect attempts at organ repair after repeated injury result in aberrant formation of extracellular matrix (ECM) and loss of tissue structure. This abnormal ECM goes from being a consequence of cellular dysregulation to become the backbone of a persistently fibrotic cell niche that compromises organic function and ultimately drives systemic disease. Here, we review our current understanding of the structure of the ECM, the mechanisms behind organ-specific fibrosis, resolution, healing and regeneration, as well as the development of anti-fibrotic strategies. We also discuss the design of biomarkers to investigate fibrosis pathophysiology, track fibrosis progression, systemic damage, and fibrosis resolution.</p>","PeriodicalId":501710,"journal":{"name":"npj Metabolic Health and Disease","volume":"3 1","pages":"25"},"PeriodicalIF":0.0000,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"npj Metabolic Health and Disease","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1038/s44324-025-00063-4","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Imperfect attempts at organ repair after repeated injury result in aberrant formation of extracellular matrix (ECM) and loss of tissue structure. This abnormal ECM goes from being a consequence of cellular dysregulation to become the backbone of a persistently fibrotic cell niche that compromises organic function and ultimately drives systemic disease. Here, we review our current understanding of the structure of the ECM, the mechanisms behind organ-specific fibrosis, resolution, healing and regeneration, as well as the development of anti-fibrotic strategies. We also discuss the design of biomarkers to investigate fibrosis pathophysiology, track fibrosis progression, systemic damage, and fibrosis resolution.
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