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.

中文翻译：

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内质网应激在动脉粥样硬化中的作用及其作为治疗靶标的潜力。

内质网（ER）压力与动脉粥样硬化和相关的心血管疾病（CVD）密切相关。它的发生是由于各种干扰ER稳态的病理因素引起的，导致ER内腔中未折叠或错误折叠的蛋白质积聚，从而导致ER功能障碍。在这里，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。讨论包括延长ER应激诱导的凋亡和炎性途径的激活，特别是在晚期病变巨噬细胞和内皮细胞（EC）中，以及在不同病变细胞中常见的与动脉粥样硬化相关的ER应激因子的激活，所有这些都有助于糖尿病的临床发展动脉粥样硬化。