The mechanism of BAF60c in myocardial metabolism through the PGC1 α/PPARα/mTOR signaling pathway in rats with heart failure.

This study explored the mechanism of BAF60c in heart failure (HF). Fetal/adult rat models of HF were established, and the levels of cardiac contractile proteins and energy metabolism-, oxidative metabolism- and glycolysis-related factors were detected. Overexpression/siRNA BAF60c plasmids were injected into adult HF rats to estimate myocardial glucose uptake, high-energy phosphate contents, mitochondrial function, and cell proliferation and apoptosis. The overexpression/siRNA BAF60c plasmids were transfected into cardiac hypertrophic H9C2 cells to explore the in vitro effects. The interaction of BAF60c and PGC1α was detected. The results suggested that adult HF rats presented increased levels of fetal proteins (ssTnI and fTnT), BAF60c and glycolysis-related factors, and reduced levels of cardiac contractile proteins, PGC1α, PPARα, and oxidative metabolism-related factors. BAF60c knockdown improved glucose uptake, maintained the oxidative metabolism/glycolysis balance, promoted H9C2 cell proliferation, and inhibited apoptosis. PGC1α interacted with BAF60c. Knocking down BAF60c also activated the PGC1α/PPARα/mTOR pathway. Overexpression of PGC1α decreased the damage to H9C2 cells caused by BAF60c. Altogether, BAF60c downregulation activated the PGC1α/PPARα/mTOR pathway, maintained the oxidative metabolism/glycolysis balance and improved mitochondrial function in rat models of HF. This study may offer novel insights into HF treatment. PMID: 33245682 [PubMed - as...
Source: Biochemistry and Cell Biology - Category: Biochemistry Authors: Tags: Biochem Cell Biol Source Type: research