Endoplasmic reticulum stress-mediated cell death in cardiovascular disease

被引:11
|
作者
An, Yajuan [1 ]
Wang, Xinshuang [1 ]
Guan, Xiuju [1 ]
Yuan, Peng [1 ]
Liu, Yue [2 ]
Wei, Liping [2 ]
Wang, Fei [3 ]
Qi, Xin [1 ,2 ]
机构
[1] Tianjin Univ Tradit Chinese Med, Sch Grad Studies, Tianjin, Peoples R China
[2] Tianjin Union Med Ctr, Dept Cardiol, Tianjin, Peoples R China
[3] Hebei Gen Hosp, Dept Vasc Surg, Shijiazhuang, Hebei, Peoples R China
来源
CELL STRESS & CHAPERONES | 2024年 / 29卷 / 01期
关键词
Endoplasmic reticulum stress; Unfolded protein responses; Cell death; Cardiovascular disease; Therapeutic strategies; UNFOLDED PROTEIN RESPONSE; XBP1; MESSENGER-RNA; ER STRESS; HEART-FAILURE; OXIDATIVE STRESS; QUALITY-CONTROL; AUTOPHAGY; APOPTOSIS; FERROPTOSIS; PATHWAY;
D O I
10.1016/j.cstres.2023.12.003
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
收藏
页码:158 / 174
页数:17
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