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Journal Article Epublish

PubMed: 40594882 DOI: 10.1038/s41598-025-06190-8

AGGF1-primed endothelial progenitor cells alleviate ischaemia-reperfusion injury in diabetic hearts.

Sci Rep 15(1):21803

Authors: Xia Li, Suwan Mu, Shuting Huang, Congcong Dai, Yumei Li, Jianqiao Li, Liang Zhong, Miaoling Wei, Liuqing Wei, Yong Li

Affiliations

  • Department of Cell Biology and Genetics, School of Intelligent Medicine and Biotechnology, Guilin Medical University, ZhiYuan Road #1, Guilin, Guangxi, China. Guangxi Key Laboratory of Brain and Cognitive Neuroscience, Guilin Medical University, Guilin, Guangxi, China.
  • Department of Cell Biology and Genetics, School of Intelligent Medicine and Biotechnology, Guilin Medical University, ZhiYuan Road #1, Guilin, Guangxi, China. Key Laboratory of Medical Biotechnology and Translational Medicine, Guilin Medical University, Guilin, Guangxi, China.
  • The Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, China.
  • The Second Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, China.
  • Department of Cell Biology and Genetics, School of Intelligent Medicine and Biotechnology, Guilin Medical University, ZhiYuan Road #1, Guilin, Guangxi, China.
  • Department of Cell Biology and Genetics, School of Intelligent Medicine and Biotechnology, Guilin Medical University, ZhiYuan Road #1, Guilin, Guangxi, China. Guangxi Key Laboratory of Brain and Cognitive Neuroscience, Guilin Medical University, Guilin, Guangxi, China. Key Laboratory of Medical Biotechnology and Translational Medicine, Guilin Medical University, Guilin, Guangxi, China. Guangxi Key Laboratory of Diabetic Systems Medicine, Guilin Medical University, Guilin, Guangxi, China.

Abstract

A number of cardioprotective pharmacological agents are not effective in diabetic hearts. The role of AGGF1-EPCs therapy in diabetic ischaemia-reperfusion(I/R) injury and the underlying mechanism by which AGGF1 regulates EPCs under hyperglycemia (HG) + hypoxia/reoxygenation (H/R) stress are still unclear. We observed that the damaging effects of HG + H/R on EPCs were abolished by AGGF1. The EPCs implantation therapy successfully restores cardiac functions, inhibits ROS production and fibrosis in diabetic I/R mice. Mechanistically, AGGF1 activates the Nrf2 and induces the activation of downstream antioxidative proteins (HO1, NQO1, and CAT). These data suggest that AGGF1 protein reverses the damaging effects of HG + H/R on EPCs via the antioxidative Nrf2. AGGF1-EPCs therapy is a novel strategy for treating diabetic I/R injury.

MeSH

Cells, Endothelial Progenitor Cells, Heart, Stem Cells, Reperfusion, Reperfusion Injury, Therapeutics