Endoplasmic reticulum stress-mediated cell death in cardiovascular disease

IF 3.3 3区生物学 Q3 CELL BIOLOGY

Cell Stress & Chaperones Pub Date : 2024-02-01 DOI:10.1016/j.cstres.2023.12.003

Yajuan An , Xinshuang Wang , Xiuju Guan , Peng Yuan , Yue Liu , Liping Wei , Fei Wang , Xin Qi

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引用次数: 0

Abstract

The endoplasmic reticulum (ER) plays a vital function in maintaining cellular homeostasis. Endoplasmic reticulum stress (ERS) can trigger various modes of cell death by activating the unfolded protein response (UPR) signaling pathway. Cell death plays a crucial role in the occurrence and development of diseases such as cancer, liver diseases, neurological diseases, and cardiovascular diseases. Several cardiovascular diseases including hypertension, atherosclerosis, and heart failure are associated with ER stress. ER stress-mediated cell death is of interest in cardiovascular disease. Moreover, an increasing body of evidence supports the potential of modulating ERS for treating cardiovascular disease. This paper provides a comprehensive review of the UPR signaling pathway, the mechanisms that induce cell death, and the modes of cell death in cardiovascular diseases. Additionally, we discuss the mechanisms of ERS and UPR in common cardiovascular diseases, along with potential therapeutic strategies.

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心血管疾病中内质网应激介导的细胞死亡。

内质网（ER）在维持细胞稳态方面发挥着重要功能。内质网应激（ERS）可通过激活未折叠蛋白反应（UPR）信号通路引发各种模式的细胞死亡。细胞死亡在癌症、肝病、神经系统疾病和心血管疾病等疾病的发生和发展中起着至关重要的作用。包括高血压、动脉粥样硬化和心力衰竭（HF）在内的多种心血管疾病都与 ER 应激有关。ER应激介导的细胞死亡在心血管疾病中很有意义。此外，越来越多的证据表明，调节 ERS 有可能治疗心血管疾病。本文全面回顾了 UPR 信号通路、诱导细胞死亡的机制以及心血管疾病中的细胞死亡模式。此外，我们还讨论了常见心血管疾病中的 ERS 和 UPR 机制以及潜在的治疗策略。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Cell Stress & Chaperones 生物-细胞生物学

CiteScore

7.60

自引率

2.60%

发文量

审稿时长

6-12 weeks

期刊介绍： Cell Stress and Chaperones is an integrative journal that bridges the gap between laboratory model systems and natural populations. The journal captures the eclectic spirit of the cellular stress response field in a single, concentrated source of current information. Major emphasis is placed on the effects of climate change on individual species in the natural environment and their capacity to adapt. This emphasis expands our focus on stress biology and medicine by linking climate change effects to research on cellular stress responses of animals, micro-organisms and plants.