CIRKIL Assembles the PKM2 Homotetramer to Exacerbate Myocardial Fibrosis after Myocardial Infarction

Key Points

• This research aims to explore how the assembly of PKM2 homotetramers contributes to myocardial fibrosis following a myocardial infarction.
• Used a myocardial infarction model in laboratory settings.
• Investigated the role of CIRKIL in assembling PKM2 into homotetramers.
• Analyzed myocardial tissue for fibrosis levels post-infarction.
• Increased myocardial fibrosis was observed in samples with PKM2 homotetramer assembly.
• Fibrosis levels were significantly correlated with PKM2 activity (p<0.05).
• Interventions that inhibited CIRKIL reduced fibrosis markers.