医学
心肌保护
伊诺斯
磷酸化
PI3K/AKT/mTOR通路
蛋白激酶B
内科学
细胞生物学
心脏病学
药理学
内分泌学
信号转导
一氧化氮
心肌梗塞
一氧化氮合酶
生物
作者
Jingyi Wu,Yifan Huang,Jing Zhang,Zujin Xiang,Jian Yang
标识
DOI:10.1016/j.ijcard.2021.12.040
摘要
We have read an interesting paper entitled “Exercise-induced late preconditioning in mice is triggered by eNOS-dependent generation of nitric oxide and activation of PKCε and is mediated by increased iNOS activity” written by Guo and his colleagues [1]. They investigated the protective role of exercise against myocardial infarction and found that exercise-induced late preconditioning depends on the phosphorylation status of eNOS at Ser1177 and subsequent NO generation and PKCε activation. Phosphorylation of eNOS-Ser(1177) is a critical event for eNOS activation, which was reported to be associated with morphometric improvement of cardiac hypertrophy and function recovery [2].
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