沉默信息调节因子3通过调节线粒体功能影响心血管疾病的研究进展OA

Cardiovascular diseases(CVD)remain the leading cause of mortality worldwide.Their complex pathogenesis is closely associated with mitochondrial dysfunction,including impaired energy metabolism,excessive oxida-tive stress,and dysregulated inflammatory responses.Increasing evidence indicates that protein acetylation is a critical post-translational modification governing mitochondrial function.Silent information regulator 3(SIRT3),the most active nicotinamide adenine dinucleotide-dependent deacetylase within the mitochondrial matrix,plays a pivotal role in maintain-ing mitochondrial homeostasis.By deacetylating multiple key mitochondrial proteins,SIRT3 regulates energy metabolism,preserves redox balance,and sustains mitochondrial structural and functional integrity.This review summarizes the molec-ular mechanisms by which SIRT3 modulates mitochondrial structure and function and highlights its involvement in the pathogenesis of major CVD,including hypertension,atherosclerosis,aneurysms,and cardiac hypertrophy.Finally,we discuss the therapeutic potential of targeting SIRT3,providing insights that may facilitate the development of novel strate-gies for the clinical management of cardiovascular diseases.