Loss of PKM2 dysregulates inflammatory signaling in the infarcted murine heart.

ABSTRACT: Inflammation and a metabolic shift from oxidative metabolism to glycolysis are common in the ischemic heart, the latter partly controlled by pyruvate kinase (muscle, PKM). We previously identified alternative splicing promoting the PKM2 isoform after myocardial infarction (MI). We examined the role of PKM2 physiological upregulation after MI, modeled by ligation of the left anterior descending coronary artery, using global PKM2 knockout (PKM2^-/-) mice. Echocardiography showed similar cardiac function between PKM2^-/- and control mice after MI. However, PKM2^-/- infarcted hearts had increased abundances of transcripts associated with oxidative stress and immune responses. Immunohistochemistry revealed greater abundance of macrophages in PKM2^-/- hear

SUBMITTER: Lee KCY 

PROVIDER: S-EPMC11705480 | biostudies-literature | 2025 Jan

REPOSITORIES: biostudies-literature