PI3K/AKT/mTOR通路
蛋白激酶B
再灌注损伤
自噬
医学
药理学
缺血
心肌梗塞
信号转导
细胞凋亡
内科学
化学
生物
细胞生物学
生物化学
作者
Ruiming Deng,Juan Zhou
标识
DOI:10.1016/j.intimp.2023.110714
摘要
Myocardial ischemia has a high incidence and mortality rate, and reperfusion is currently the standard intervention. However, reperfusion may lead to further myocardial damage, known as myocardial ischemia/reperfusion injury (MIRI). There are currently no effective clinical treatments for MIRI. The PI3K/Akt signaling pathway is involved in cardiovascular health and disease and plays an important role in reducing myocardial infarct size and restoring cardiac function after MIRI. Activation of the PI3K/Akt pathway provides myocardial protection through synergistic upregulation of antioxidant, anti-inflammatory, and autophagy activities and inhibition of mitochondrial dysfunction and cardiomyocyte apoptosis. Many studies have shown that PI3K/Akt has a significant protective effect against MIRI. Here, we reviewed the molecular regulation of PI3K/Akt in MIRI and summarized the molecular mechanism by which PI3K/Akt affects MIRI, the effects of ischemic preconditioning and ischemic postconditioning, and the role of related drugs or activators targeting PI3K/Akt in MIRI, providing novel insights for the formulation of myocardial protection strategies. This review provides evidence of the role of PI3K/Akt activation in MIRI and supports its use as a therapeutic target.
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