Scholarlink

<p>Diabetic cardiomyopathy (DCM) represents a prevalent and clinically significant complication associated with diabetes mellitus, characterized by myocardial dysfunction in the absence of overt coronary artery disease or hypertension. Consequently, there is an urgent need for novel preventive and therapeutic strategies. Sirtuin 3 (SIRT3), a member of the sirtuin family and a mitochondrial nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, has emerged as a pivotal regulator of mitochondrial function, oxidative stress, and cellular metabolism. In diabetic hearts, the activity and expression of SIRT3 are consistently diminished due to various regulators, including exercise, noncoding RNAs, and metabolic enzymes. This review elucidates the role of SIRT3 in regulating mitochondrial homeostasis, oxidative stress/inflammation, and lipotoxicity, thereby contributing to the progression of DCM. Furthermore, we provide a comprehensive overview of the modulators targeting SIRT3 as potential therapeutic agents to mitigate DCM. In conclusion, targeting SIRT3 is a novel and promising approach for combating DCM.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Targeting SIRT3 in Diabetic Cardiomyopathy: Mechanism-Based Therapeutic Strategies

  • 期刊论文

  • 发表日期：

    2026年2月24日

查看全文
  • Xiaofang Zhang,
  • Hui Lin,
  • Xinrou Yu,
  • Tiantian Lu,
  • Jun Wang,
  • Hui Ji,
  • Dihua Huang,
  • Dajun Lou

摘要

Diabetic cardiomyopathy (DCM) represents a prevalent and clinically significant complication associated with diabetes mellitus, characterized by myocardial dysfunction in the absence of overt coronary artery disease or hypertension. Consequently, there is an urgent need for novel preventive and therapeutic strategies. Sirtuin 3 (SIRT3), a member of the sirtuin family and a mitochondrial nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, has emerged as a pivotal regulator of mitochondrial function, oxidative stress, and cellular metabolism. In diabetic hearts, the activity and expression of SIRT3 are consistently diminished due to various regulators, including exercise, noncoding RNAs, and metabolic enzymes. This review elucidates the role of SIRT3 in regulating mitochondrial homeostasis, oxidative stress/inflammation, and lipotoxicity, thereby contributing to the progression of DCM. Furthermore, we provide a comprehensive overview of the modulators targeting SIRT3 as potential therapeutic agents to mitigate DCM. In conclusion, targeting SIRT3 is a novel and promising approach for combating DCM.