Angiotensin II-induced cardiac fibrosis and dysfunction are exacerbated by deletion of cGKI in periostin+ myofibroblasts.

ABSTRACT: Differentiation of cardiac fibroblasts (CF) into myofibroblasts (CMFs) is considered a critical event in response to the maladaptive cardiac remodeling triggered by angiotensin II (Ang II). Active CMFs are proliferative and contribute to the production of extracellular matrix and matricellular proteins such as periostin, to myocardial fibrosis and thus muscle stiffness. Although previous studies provided substantial evidence for the antifibrotic signaling elicited by NO/NP-cGMP-cGKI, the role of this axis in modulating CMF function(s) in vivo remains unclear.To address this, Ang II was delivered through osmotic minipumps into tamoxifen-induced CMF-specific cGKI knockout (cmfKO) and littermate control (CTR) male mice. CMF-restricted Cre activity in periostin+ cells resulted in an effective

SUBMITTER: Santos MC 

PROVIDER: S-EPMC12247847 | biostudies-literature | 2025 Apr

REPOSITORIES: biostudies-literature