Yang Shengjie, Wu Min, Li Xiaoya, Zhao Ran, Zhao Yixi, Liu Longtao, Wang Songzi
Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
Beijing University of Chinese Medicine, Beijing, China.
Oxid Med Cell Longev. 2020 Sep 9;2020:9270107. doi: 10.1155/2020/9270107. eCollection 2020.
Endoplasmic reticulum (ER) stress is closely associated with atherosclerosis and related cardiovascular diseases (CVDs). It occurs due to various pathological factors that interfere with ER homeostasis, resulting in the accumulation of unfolded or misfolded proteins in the ER lumen, thereby causing ER dysfunction. Here, we discuss the role of ER stress in different types of cells in atherosclerotic lesions. This discussion includes the activation of apoptotic and inflammatory pathways induced by prolonged ER stress, especially in advanced lesional macrophages and endothelial cells (ECs), as well as common atherosclerosis-related ER stressors in different lesional cells, which all contribute to the clinical progression of atherosclerosis. In view of the important role of ER stress and the unfolded protein response (UPR) signaling pathways in atherosclerosis and CVDs, targeting these processes to reduce ER stress may be a novel therapeutic strategy.
内质网（ER）应激与动脉粥样硬化及相关心血管疾病（CVD）密切相关。它是由多种干扰内质网稳态的病理因素引起的，导致内质网腔中未折叠或错误折叠蛋白质的积累，从而引起内质网功能障碍。在此，我们讨论内质网应激在动脉粥样硬化病变中不同类型细胞中的作用。这种讨论包括长期内质网应激诱导的凋亡和炎症途径的激活，特别是在晚期病变巨噬细胞和内皮细胞（EC）中，以及不同病变细胞中常见的与动脉粥样硬化相关的内质网应激源，所有这些都促成了动脉粥样硬化的临床进展。鉴于内质网应激和未折叠蛋白反应（UPR）信号通路在动脉粥样硬化和心血管疾病中的重要作用，针对这些过程以减轻内质网应激可能是一种新的治疗策略。
