Pyruvate kinase splice variants in fibroblasts influence cardiac remodeling after myocardial infarction in male mice.

ABSTRACT: Fibroblasts are crucial for cardiac repair after myocardial infarction (MI). In response to signaling cues, they differentiate to phenotypes with robust capacities to synthesize and secrete extracellular matrix (ECM) and signaling molecules. Although activated fibroblast phenotypes are associated with pronounced changes in metabolism, it remains unclear how the metabolic network upholds the effector functions of fibroblasts in the infarcted heart. We found that two enzymes that could facilitate a phosphoenolpyruvate cycle, i.e. pyruvate kinase muscle isoform 2 (PKM2) and phosphoenolpyruvate carboxykinase 2 (PCK2), are elevated in the heart after MI. Although Pck2 deletion had no effect on post-MI remodeling, fibroblast-specific switching of Pkm2 to Pkm1 (fbPkm2 → 1) mitigated ventricular d

SUBMITTER: Wells CK 

PROVIDER: S-EPMC12344556 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature