{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Walker CJ"],"funding":["American Heart Association","Human Frontiers Science Program fellowship","Burroughs Wellcome Fund","NHLBI NIH HHS","NIAMS NIH HHS","U.S. Department of Health & Human Services | National Institutes of Health","NIGMS NIH HHS","NIH HHS","National Science Foundation","US department of education"],"pagination":["1485-1499"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9102466"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["5(12)"],"pubmed_abstract":["Fibrotic disease is caused by the continuous deposition of extracellular matrix by persistently activated fibroblasts (also known as myofibroblasts), even after the resolution of the injury. Using fibroblasts from porcine aortic valves cultured on hydrogels that can be softened via exposure to ultraviolet light, here we show that increased extracellular stiffness activates the fibroblasts, and that cumulative tension on the nuclear membrane and increases in the activity of histone deacetylases transform transiently activated fibroblasts into myofibroblasts displaying condensed chromatin with genome-wide alterations. The condensed structure of the myofibroblasts is associated with cytoskeletal stability, as indicated by the inhibition of chromatin condensation and myofibroblast persistence "],"journal":["Nature biomedical engineering"],"pubmed_title":["Nuclear mechanosensing drives chromatin remodelling in persistently activated fibroblasts."],"pmcid":["PMC9102466"],"funding_grant_id":["T32 HL007822‐20","R01 AR063712","R01 HL132353","T32 HL007822","RHL117138-05","R21 AR066230","R01 HL117138","S10 OD012300","R01 GM29090","GM125871","R25 HL145817","F31HL142223","20POST3521111","R21 AR067469","K99 HL148542","T32 GM065103","T32 HL007444","F31 HL142223","1144807","R01 GM125871","R01 GM029090"],"pubmed_authors":["Allen MA","Clark K","Grim JC","Ramirez D","Crocini C","Killaars AR","Dowell RD","Anseth KS","Aguado BA","Leinwand LA","Walker CJ"],"additional_accession":[]},"is_claimable":false,"name":"Nuclear mechanosensing drives chromatin remodelling in persistently activated fibroblasts.","description":"Fibrotic disease is caused by the continuous deposition of extracellular matrix by persistently activated fibroblasts (also known as myofibroblasts), even after the resolution of the injury. Using fibroblasts from porcine aortic valves cultured on hydrogels that can be softened via exposure to ultraviolet light, here we show that increased extracellular stiffness activates the fibroblasts, and that cumulative tension on the nuclear membrane and increases in the activity of histone deacetylases transform transiently activated fibroblasts into myofibroblasts displaying condensed chromatin with genome-wide alterations. The condensed structure of the myofibroblasts is associated with cytoskeletal stability, as indicated by the inhibition of chromatin condensation and myofibroblast persistence ","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Dec","modification":"2026-06-04T04:53:23.304Z","creation":"2025-02-18T23:35:52.49Z"},"accession":"S-EPMC9102466","cross_references":{"pubmed":["33875841"],"doi":["10.1038/s41551-021-00709-w"]}}