Leng Yiming, Zhang Ying, Li Xinyu, Wang Zeyu, Zhuang Quan, Lu Yao
Clinical Research Center of the 3rd Xiangya Hospital, Central South University, Changsha, China.
Transplantation Center of the 3rd Xiangya Hospital, Central South University, Changsha, China.
Front Pharmacol. 2021 Nov 18;12:762334. doi: 10.3389/fphar.2021.762334. eCollection 2021.
The receptor interacting protein kinases 1/3 (RIPK1/3) have emerged as the key mediators in cell death pathways and inflammatory signaling, whose ubiquitination, phosphorylation, and inhibition could regulate the necroptosis and apoptosis effectually. Recently, more and more studies show great interest in the mechanisms and the regulator of RIPK1/3-mediated inflammatory response and in the physiopathogenesis of cardiovascular diseases. The crosstalk of autophagy and necroptosis in cardiomyocyte death is a nonnegligible conversation of cell death. We elaborated on RIPK1/3-mediated necroptosis, pathways involved, the latest regulatory molecules and therapeutic targets in terms of ischemia reperfusion, myocardial remodeling, myocarditis, atherosclerosis, abdominal aortic aneurysm, and cardiovascular transplantation, etc.
受体相互作用蛋白激酶1/3(RIPK1/3)已成为细胞死亡途径和炎症信号传导中的关键介质,其泛素化、磷酸化及抑制作用可有效调节坏死性凋亡和凋亡。最近,越来越多的研究对RIPK1/3介导的炎症反应机制及其调节因子以及心血管疾病的病理生理发病机制表现出极大兴趣。心肌细胞死亡中自噬与坏死性凋亡的相互作用是细胞死亡中不可忽视的话题。我们从缺血再灌注、心肌重塑、心肌炎、动脉粥样硬化、腹主动脉瘤和心血管移植等方面阐述了RIPK1/3介导的坏死性凋亡、相关途径、最新调节分子和治疗靶点。