Related Experiment Video
Updated: Aug 20, 2025
Herbal Munziq Ameliorates Myocardial Ischemia-Reperfusion Injury by Inhibiting Inflammation
Published on: January 10, 2025
C1q/TNF-related protein-2 improved angiogenesis to protect myocardial function during ischaemia‒reperfusion
Mingfang Ye1, Qi-Hong Wu2, Ke Yang3
1Department of Cardiology, 117890Fujian Medical University Union Hospital, Fujian Medical Center for Cardiovascular Diseases, Fujian Institute of Coronary Heart Disease, Fujian Key Laboratory of Vascular Aging, Fujian Medical University, Fujian, China.
Background:
Collateral growth plays an important role in the recovery of acute myocardial infarction. C1q/TNF-related protein-2 (CTRP2), a CTRP family member, showed some protective effects on cell survival. In this study, the relationship between CTRP2 and collateral growth was examined.
Methods:
C57BL/6 mice were subjected to myocardial ischaemia/reperfusion (I/R), and the expression of CTRP2 and the effect of CTRP2 on infarction size, cardiac function and angiogenesis were examined. The ischaemic hindlimb model was also used to examine the effect of CTRP2. In vitro, CTRP2-mediated regulation of angiogenesis, AKT activation and VEGFR2 expression in endothelial cells was examined. The CTRP2 level associated with good collateral growth was observed in a cohort.
Results:
I/R reduced CTRP2 expression, and intraperitoneal injection of recombinant CTRP2 protein improved infarction size, cardiac function and angiogenesis. Overexpression of CTRP2 promoted blood refusion and collateral growth in ischaemic hindlimb mice. In vitro, CTRP2 enhanced tube formation and migration in a dose-dependent manner, while CTRP2 increased AKT phosphorylation and VEGFR2 expression. In an observational clinical cohort, CTRP2 levels were significantly increased in patients with good collateral growth, and CTRP2 was negatively associated with poor collateral growth in patients.
Conclusion:
CTRP2 improved cardiac function by promoting collateral growth by promoting AKT-VEGFR2.
