程序性细胞坏死在心肌缺血中的研究进展

Research progress on programmed cell necroptosis in myocardial ischemia

程序性细胞死亡在个体发育和维持自身稳态中起着至关重要的作用。近年研究表明,心肌缺血和缺血再灌注损伤中有程序性坏死机制的参与,它是受细胞内信号通路严密调控的主动过程,其中,受体相互作用蛋白激酶(RIPK)1和3、混合谱系激酶域样蛋白(MLKL)和钙离子/钙调蛋白依赖性蛋白激酶Ⅱ(CaMKⅡ)发挥着极其重要的功能。本文综述了这些关键分子在心肌缺血中的研究进展,并探讨了靶向程序性坏死信号的药物开发状况。

Programmed cell death plays a vital role in ontogeny and homeostasis.Recent studies have shown that programmed cell necroptosis is involved in myocardial ischemia and ischemia-reperfusion injury,which is an active process closely regulated by intracellular signaling pathways.Among them,receptor interaction protein kinase(RIPK)1 and 3,mixed lineage kinase domain-like protein(MLKL)and calcium/calmodulin dependent protein kinaseⅡ(CaMKⅡ)play extremely important functions.In this paper,we reviewed the research progress of these key molecules in myocardial ischemia,and discussed the drug development status of targeting programmed cell necroptotic signaling.