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CD38 Deficiency Protects Heart from High Fat Diet-Induced Oxidative Stress Via Activating Sirt3/FOXO3 Pathway

Ling-Fang Wang1, Cong-Cong Huang1, Yun-Fei Xiao1,2

  • 1Institute of Translational Medicine, Nanchang University, Nanchang, China.

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
|August 17, 2018
PubMed

Insights

CD38 deficiency protects the heart from high-fat diet injury by reducing oxidative stress. This occurs through the Sirt3/FOXO3 pathway, enhancing antioxidant defenses and improving metabolic health in cardiac tissue.

Area of Science:

  • Cardiovascular Biology
  • Metabolic Disorders
  • Molecular Mechanisms of Disease

Background:

  • CD38 deficiency previously showed cardioprotective effects against ischemia/reperfusion and high-fat diet (HFD)-induced obesity.
  • The specific role of CD38 in HFD-induced cardiac injury remained largely undetermined.

Purpose of the Study:

  • To investigate the protective effects and underlying mechanisms of CD38 deficiency in HFD-induced heart injury.
  • To elucidate the impact of CD38 on cardiac metabolism and oxidative stress under HFD conditions.

Main Methods:

  • Metabolomics analysis of heart tissue from wild-type (WT) and CD38 knockout (CD38-/-) mice fed HFD.
  • In vitro studies using H9C2 cells to assess cell viability, LDH release, ROS production, and lipid synthesis after CD38 knockdown and oleic acid (OA) stimulation.
  • Quantitative PCR (QPCR) to analyze gene expression related to oxidative stress and metabolic pathways.

Main Results:

  • CD38 deficiency in HFD-fed mice led to increased intracellular glutathione (GSH) and NAD+ levels, alongside decreased free fatty acids.
  • In vitro, CD38 knockdown attenuated OA-induced cellular injury, ROS production, and lipid accumulation.
  • Upregulation of the Sirt3/FOXO3/SOD2 antioxidant pathway and downregulation of NOX2/NOX4 were observed in CD38-deficient or knockdown cells.

Conclusions:

  • CD38 deficiency confers protection against HFD-induced cardiac oxidative stress.
  • The protective mechanism involves the activation of the Sirt3/FOXO3-mediated anti-oxidative stress pathway.
  • Targeting CD38 may represent a novel therapeutic strategy for managing HFD-related heart conditions.
Abstract

Keywords:
Cd38Heart Oleic acidOxidative stressSirt3/FOXO3 pathway

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