坏死性下垂
细胞生物学
线粒体通透性转换孔
再灌注损伤
信号转导
磷酸化
程序性细胞死亡
化学
钙调蛋白
缺血
细胞凋亡
生物
医学
钙
内科学
生物化学
有机化学
作者
Junhao Li,Zhang Jia-ji,Yunlong Zhong,Dong-Ge Xie,Han Han,Zhongqing Zhang,Liu Y,Shoutian Li
标识
DOI：10.1016/j.cellsig.2024.111344
摘要
Myocardial ischemia-reperfusion injury (MIRI) frequently complicates postoperative cardiovascular disease treatment. Necroptosis, a cell death mechanism similar to apoptosis, is regulated by specific signaling pathways and plays an important role in MIRI. Receptor-interacting protein 3 (RIP3), a key protein regulating necroptosis during MIRI, directly phosphorylates calmodulin-dependent protein kinase II (CaMKII). Leading to mitochondrial permeablity transition pore (mPTP) opening and inducing necroptosis. Transient receptor potential canonical channel 6 (TRPC6) regulats Ca
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