Department of Clinical Laboratory, Xi'an No 5 Hospital, No. 112 West Main Street, Lianhu District, Xi'an, 710082, Shaanxi, China.
The Five Ward of Internal Medicine, Xi'an No 5 Hospital, Xi'an, 710082, Shaanxi, China.
Mol Cell Biochem. 2021 Feb;476(2):775-783. doi: 10.1007/s11010-020-03943-z. Epub 2020 Oct 21.
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.
心肌梗死（MI）是由持续缺血缺氧引起的心肌坏死性疾病。醛缩酶 A（ALDOA）的异常表达已在心肌肥厚、心力衰竭和其他心脑血管疾病中报道。本研究旨在探讨 ALDOA 对缺氧/再灌注（H/R）诱导的氧化应激的影响，并探讨其潜在机制。在 MI 患者的血液样本和 H/R 诱导的 H9C2 心肌细胞中，ALDOA 的表达水平较低。ALDOA 的过表达抑制了 H/R 诱导的氧化应激和细胞凋亡。通过共免疫沉淀和蛋白印迹实验，我们证明 ALDOA 通过上调 VEGF 来调节 Notch1-Jagged1 信号通路。总之，我们的数据表明，ALDOA 通过 VEGF/Notch1/Jagged1 轴保护心肌细胞免受 H/R 诱导的氧化应激，应该作为未来 MI 治疗的潜在治疗靶点进行研究。
