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Hyperglycemia-induced SIRT3 inhibition contributes to diabetic cardiomyopathy by impairing Cav-3-mediated mitophagy

Zhenshuai Jin1, Yanwei Ji1, Wating Su1

  • 1Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, China.

Biochemical Pharmacology
|February 22, 2026
PubMed

Insights

Diabetic cardiomyopathy (DCM) involves impaired mitophagy. This study reveals hyperglycemia-induced Sirtuin 3 (SIRT3) suppression impairs caveolin-3 (Cav-3)-mediated mitophagy, contributing to DCM pathogenesis.

Area of Science:

  • Cardiovascular Biology
  • Metabolic Disorders
  • Cellular Biology

Background:

  • Diabetic cardiomyopathy (DCM) is a significant cause of mortality in diabetes.
  • Impaired mitophagy is a key factor in DCM pathogenesis.
  • The roles of Sirtuin 3 (SIRT3) and caveolin-3 (Cav-3) in mitophagy and DCM require further elucidation.

Purpose of the Study:

  • To investigate the interplay between SIRT3, Cav-3, and mitophagy in the context of DCM.
  • To determine the specific mechanisms by which SIRT3 and Cav-3 influence mitophagy in diabetic conditions.

Main Methods:

  • Utilized diabetic C57BL/6 mice and Cav-3 knockout (Cav-3 KO) mice models.
  • Employed cultured H9C2 cardiomyocytes treated with high glucose (HG).
  • Investigated the effects of SIRT3 and Cav-3 knockdown (siRNA) and overexpression.

Main Results:

  • Diabetic mice exhibited impaired cardiac function, reduced mitophagy, and decreased SIRT3 and Cav-3 expression.
  • Cav-3 KO diabetic mice showed exacerbated cardiac dysfunction and mitophagy impairment.
  • SIRT3 knockdown worsened HG-induced cardiomyocyte damage and reduced mitophagy, decreasing Cav-3 expression; Cav-3 overexpression rescued these effects.

Conclusions:

  • Hyperglycemia-induced SIRT3 suppression contributes to DCM.
  • SIRT3 functions upstream of Cav-3, impairing Cav-3-mediated mitophagy.
  • Targeting the SIRT3-Cav-3 pathway may offer therapeutic strategies for DCM.
Keywords:
Cav-3DiabetesDiabetic cardiomyopathyMitophagySIRT3

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