Mitochondrial proteins in heart failure: The role of deacetylation by SIRT3

Abstract

Heart failure (HF) is still the leading cause of death worldwide, occurring with a variety of complex mechanisms. However, most intervention for HF do not directly target the pathological mechanisms underlying cell damage in failing cardiomyocytes. Mitochondria are involved in many physiological processes, which is an important guarantee for normal heart function. Mitochondrial dysfunction is considered to be the critical node of the development of HF. Strict modulation of the mitochondrial function can ameliorate the myocardial injury and protect cardiac function. Acetylation plays an important role in mitochondrial protein homeostasis, and SIRT3, the most important deacetylation protein in mitochondria, is involved in the maintenance of mitochondrial function. SIRT3 can delay the progression of HF by improving mitochondrial function. Herein we summarize the interaction between SIRT3 and proteins related to mitochondrial function including oxidative phosphorylation (OXPHOS), fatty acid oxidation (FAO), mitochondrial biosynthesis, mitochondrial quality control. In addition, we also sum up the effects of this interaction on HF and the research progress of treatments targeting SIRT3, so as to find potential HF therapeutic for clinical use in the future.

Keywords: Deacetylation; Heart failure; Mitochondria; SIRT3.