ALDOA protects cardiomyocytes against H/R-induced apoptosis and oxidative stress by regulating the VEGF/Notch 1/Jagged 1 pathway.

Myocardial infarction (MI) is a myocardial necrosis disease caused by continuous ischemia and hypoxia. Abnormal expression of aldolase A (ALDOA) has been reported in cardiac hypertrophy, heart failure and other cardio-cerebrovascular diseases. The present study aims to explore the effects of ALDOA on hypoxia/reperfusion (H/R)-induced oxidative stress, and investigate the underlying mechanisms. ALDOA was expressed at a low level in blood samples from MI patients and H/R-induced H9C2 cardiomyocytes. Overexpression of ALDOA suppressed H/R-induced oxidative stress and apoptosis. Using co-immunoprecipitation and protein blots, we demonstrated that ALDOA modulates the Notch 1-Jagged 1 signalling pathway by upregulating VEGF. Taken together, our data reveal that ALDOA protects cardiomyocytes from H/R-induced oxidative stress through the VEGF/Notch 1/Jagged 1 axis, and should be investigated as a therapeutic target for the treatment of MI in future.