蛋白激酶在慢性低氧的心脏保护效应中的作用。
The involvement of protein kinases in the cardioprotective effect of chronic hypoxia.
机构信息
Cardiology Research Institute, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk, Russia.
出版信息
Physiol Res. 2020 Dec 22;69(6):933-945. doi: 10.33549/physiolres.934439. Epub 2020 Nov 2.
The purpose of this review is to analyze the involvement of protein kinases in the cardioprotective mechanism induced by chronic hypoxia. It has been reported that chronic intermittent hypoxia contributes to increased expression of the following kinases in the myocardium: PKCdelta, PKCalpha, p-PKCepsilon, p-PKCalpha, AMPK, p-AMPK, CaMKII, p-ERK1/2, p-Akt, PI3-kinase, p-p38, HK-1, and HK-2; whereas, chronic normobaric hypoxia promotes increased expression of the following kinases in the myocardium: PKCepsilon, PKCbetaII, PKCeta, CaMKII, p-ERK1/2, p-Akt, p-p38, HK-1, and HK-2. However, CNH does not promote enhanced expression of the AMPK and JNK kinases. Adaptation to hypoxia enhances HK-2 association with mitochondria and causes translocation of PKCdelta, PKCbetaII, and PKCeta to the mitochondria. It has been shown that PKCdelta, PKCepsilon, ERK1/2, and MEK1/2 are involved in the cardioprotective effect of chronic hypoxia. The role of other kinases in the cardioprotective effect of adaptation to hypoxia requires further research.
本次综述旨在分析蛋白激酶在慢性低氧诱导的心肌保护机制中的作用。已有报道称，慢性间歇性低氧有助于增加心肌中以下蛋白激酶的表达：PKCdelta、PKCalpha、p-PKCepsilon、p-PKCalpha、AMPK、p-AMPK、CaMKII、p-ERK1/2、p-Akt、PI3-kinase、p-p38、HK-1 和 HK-2；而慢性常压低氧则促进心肌中以下蛋白激酶的表达增加：PKCepsilon、PKCbetaII、PKCeta、CaMKII、p-ERK1/2、p-Akt、p-p38、HK-1 和 HK-2。然而，CNH 并不促进 AMPK 和 JNK 激酶的增强表达。适应低氧增强了 HK-2 与线粒体的结合，并导致 PKCdelta、PKCbetaII 和 PKCeta 向线粒体的易位。已有研究表明，PKCdelta、PKCepsilon、ERK1/2 和 MEK1/2 参与了慢性低氧的心肌保护作用。其他激酶在适应低氧的心肌保护作用中的作用需要进一步研究。
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