Targeting the E Prostanoid Receptor EP4 Mitigates Cardiac Fibrosis Induced by β-Adrenergic Activation.

ABSTRACT: Sustained β-adrenergic activation induces cardiac fibrosis characterized by excessive deposition of extracellular matrix (ECM). Prostaglandin E₂ (PGE₂) receptor EP4 is essential for cardiovascular homeostasis. This study aims to investigate the roles of cardiomyocyte (CM) and cardiac fibroblast (CF) EP4 in isoproterenol (ISO)-induced cardiac fibrosis. By crossing the EP4^f/f mice with α-MyHC-Cre or S100A4-Cre mice, this work obtains the CM-EP4 knockout (EP4^f/f-α-MyHC^Cre+) or CF-EP4 knockout (EP4^f/f-S100A4^Cre+) mice. The mice of both genders are subcutaneously injected with ISO (5 mg kg^-1 day^-1) for 7 days. Compared to the control mice, both EP4^f/f-α-MyHC^Cre+ and EP4^f

SUBMITTER: Xu H 

PROVIDER: S-EPMC11948031 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature