内质网应激相关心肌细胞凋亡研究进展

Research Advances in Endoplasmic Reticulum Stress-Related Cardiomyocyte Apoptosis

摘要: 营养缺乏、缺氧、缺血、氧化应激和DNA损伤等情况能引起内质网腔内错误折叠或未折叠蛋白的积累，即形成内质网应激，随后通过未折叠蛋白反应对机体产生促生存或促凋亡作用。现综述内质网应激和未折叠蛋白反应的定义、未折叠蛋白反应相关的信号通路、内质网应激诱导心肌细胞凋亡的途径、通过调节内质网应激减轻心肌细胞凋亡，以期为心血管疾病的新型治疗提供策略。

Abstract: Nutrient deficiency, hypoxia, ischemia, oxidative stress, and DNA damage can cause the accumula-tion of misfolded or unfolded proteins in the endoplasmic reticulum cavity, that is, the formation of endoplasmic reticulum stress, followed by a pro-survival or pro-apoptotic effect on the body through the response of unfolded proteins. The definitions of endoplasmic reticulum stress and un-folded protein responses, the signaling pathways associated with unfolded protein responses, the pathways by which endoplasmic reticulum stress induces apoptosis of cardiomyocytes, and the re-duction of cardiomyocyte apoptosis by regulating endoplasmic reticulum stress are reviewed in or-der to provide strategies for novel treatments for cardiovascular diseases.