Prostaglandin I₂ signaling prevents angiotensin II-induced atrial remodeling and vulnerability to atrial fibrillation in mice.

ABSTRACT: Atrial fibrillation (AF) is the most common arrhythmia, and atrial fibrosis is a pathological hallmark of structural remodeling in AF. Prostaglandin I₂ (PGI₂) can prevent the process of fibrosis in various tissues via cell surface Prostaglandin I₂ receptor (IP). However, the role of PGI₂ in AF and atrial fibrosis remains unclear. The present study aimed to clarify the role of PGI₂ in angiotensin II (Ang II)-induced AF and the underlying molecular mechanism. PGI₂ content was decreased in both plasma and atrial tissue from patients with AF and mice treated with Ang II. Treatment with the PGI₂ analog, iloprost, reduced Ang II-induced AF and atrial fibrosis. Iloprost prevented Ang II-induced atrial fibroblast collagen

SUBMITTER: Zhang Y 

PROVIDER: S-EPMC11335301 | biostudies-literature | 2024 Jun

REPOSITORIES: biostudies-literature