Histone Deacetylase 6 Controls Atrial Fibrosis and Remodeling in Postinfarction Mice Through the Modulation of Wnt3a/GSK-3β Signaling.

ABSTRACT: Myocardial infarction (MI)-induced hemodynamic disorder often causes atrial structural and electrophysiological remodeling. Given that histone deacetylase 6 (HDAC6) plays important roles in pathobiology, we investigated the molecular mechanism underlying MI-induced atrial remodeling in mice, with a special focus on HDAC6-mediated Wnt3a/GSK3β signaling activation. We observed an upregulation of HDAC6 expression in the left atria of mice at 2 weeks post-MI, accompanied by atrial enlargement, increased atrial fibrosis and inflammation, myocyte hypertrophy, impaired mitochondrial biogenesis, elevated levels of Wnt3a, GSK3β, and β-catenin protein, and reduced gap junction CX43 expression; these alterations were reversed by HDAC6 deletion. This atrialoprotective effect was mimicked by HDAC6 inhi

SUBMITTER: Shu S 

PROVIDER: S-EPMC12083057 | biostudies-literature | 2025 May

REPOSITORIES: biostudies-literature