Li Xia, Mu Suwan, Huang Shuting, Dai Congcong, Li Yumei, Li Jianqiao, Zhong Liang, Wei Miaoling, Wei Liuqing, Li Yong
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.
Sci Rep. 2025 Jul 1;15(1):21803. doi: 10.1038/s41598-025-06190-8.
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.
许多心脏保护药物对糖尿病心脏无效。AGGF1-EPCs疗法在糖尿病缺血再灌注（I/R）损伤中的作用以及AGGF1在高血糖（HG）+缺氧/复氧（H/R）应激下调节EPCs的潜在机制仍不清楚。我们观察到AGGF1消除了HG + H/R对EPCs的损伤作用。EPCs植入疗法成功恢复了糖尿病I/R小鼠的心脏功能，抑制了活性氧生成和纤维化。机制上，AGGF1激活Nrf2并诱导下游抗氧化蛋白（HO1、NQO1和CAT）的激活。这些数据表明，AGGF1蛋白通过抗氧化的Nrf2逆转了HG + H/R对EPCs的损伤作用。AGGF1-EPCs疗法是治疗糖尿病I/R损伤的一种新策略。
