Mitophagy: A Potential Target for Pressure Overload-Induced Cardiac Remodelling

Figure 3

Mitochondrial dynamics in pressure overload model. In the pressure overload model, MFN2 was downregulated. After TAC, Mir-17-5p and Mir-106a inhibit MFN2 and cause cardiac hypertrophy. In OPA1+/- mice, TAC results in more severe cardiac remodelling and cardiac dysfunction. Increased expression of OPA1 by upregulating YME1L or TNFR2 protects hearts from pressure overload. The decreased level phosphorylation at s616 of DRP1 accompanies a decrease in mitophagy. Knockout of DRP1 aggravates mitochondrial dysfunction, cardiac hypertrophy, and cardiac dysfunction caused by pressure overload. STAT1 promotes mitochondrial division through UCP2/P-DRP1 pathway to resist TAC-induced myocardial hypertrophy. However, the use of DRP1 inhibitor Mdivi-1 improves cardiac dysfunction and cardiac remodelling after TAC.