{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,16]],"date-time":"2026-03-16T07:11:44Z","timestamp":1773645104841,"version":"3.50.1"},"reference-count":48,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,3,16]],"date-time":"2026-03-16T00:00:00Z","timestamp":1773619200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Pharmacol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Myocardial fibrosis, characterized by excessive collagen deposition and fibroblast activation, is a pivotal pathological process driving heart failure after myocardial infarction (MI). Our prior research revealed that Brahma-related gene 1 (BRG1) expression is elevated after MI and exacerbated cardiac electrophysiological remodeling; however, its precise role and molecular mechanism in post-MI fibrosis remain undefined.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      BRG1 expression was assessed in a mouse MI model and in TGF-\u03b21-stimulated cardiac fibroblasts (CFs). Gain- and loss-of-function studies were performed using adenoviral vectors, siRNA, and plasmids\n                      <jats:italic>in vitro<\/jats:italic>\n                      and\n                      <jats:italic>in vivo<\/jats:italic>\n                      . Cardiac function and fibrosis were evaluated by echocardiography and histology. The molecular mechanism was dissected through co-immunoprecipitation (Co-IP), dual-luciferase reporter assays, chromatin immunoprecipitation (ChIP), and functional rescue experiments targeting the PP2A\/Smad3 axis.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      BRG1 was upregulated in fibrotic mouse hearts post-MI and in activated CFs.\n                      <jats:italic>In vivo<\/jats:italic>\n                      , BRG1 knockdown via AAV9-shRNA improved cardiac function, reduced infarct size, and attenuated fibrosis.\n                      <jats:italic>In vitro<\/jats:italic>\n                      , BRG1 promoted CFs proliferation, migration, and collagen production. Mechanistically, TGF-\u03b21 enhanced the interaction between BRG1 and the transcription factor ZEB1. This complex transcriptionally repressed\n                      <jats:italic>Ppp2r1a<\/jats:italic>\n                      , the gene encoding the PP2A structural subunit A\u03b1, leading to diminished PP2A activity. Consequently, Smad3 phosphorylation and nuclear translocation were enhanced, amplifying the pro-fibrotic TGF-\u03b2\/Smad3 cascade. Crucially, ZEB1 knockdown or PP2A inhibition (okadaic acid) could respectively block or rescue the fibrotic effects of BRG1. Finally, BRG1 knockdown similarly suppressed fibrotic activation in human CFs.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Our study defines a novel BRG1\/ZEB1\/PP2A transcriptional axis as a key driver of myocardial fibrosis and suggests BRG1 as a potential therapeutic target for mitigating fibrotic remodeling after MI.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fphar.2026.1802700","type":"journal-article","created":{"date-parts":[[2026,3,16]],"date-time":"2026-03-16T06:39:53Z","timestamp":1773643193000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["BRG1 exacerbates myocardial fibrosis after myocardial infarction by interacting with 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