期刊
NATURE REVIEWS CARDIOLOGY
卷 18, 期 7, 页码 499-521出版社
NATURE PORTFOLIO
DOI: 10.1038/s41569-021-00511-w
关键词
-
资金
- National Key R&D Program of China [2017YFA0506000]
- University of Wyoming
- FONDECYT [11180186]
- FONDAP program [ANID/FONDAP/15150012]
- Millennium Institute [P09-015-F]
- European Commission RD MSCA-RISE [734749]
- Natural Science Foundation of China [91749128, 81770261, 81521001]
- Science and Technology Innovation Project of the Chinese Academy of Medical Sciences (Health and Longevity Pilot Special Project) [2019-RC-HL-021]
- Training Program of Excellent Academic Leaders of Shanghai Health Mission [2018BR25]
- Marie Curie Actions (MSCA) [734749] Funding Source: Marie Curie Actions (MSCA)
This review summarizes the role of endoplasmic reticulum stress and protein response in cardiovascular diseases, discussing potential therapeutic strategies for restoring ER proteostasis.
In this Review, Ren and colleagues summarize the latest advances in understanding the unfolded protein response and endoplasmic reticulum stress in the pathogenesis of cardiovascular disease and discuss potential therapeutic strategies aimed at restoring endoplasmic reticulum proteostasis in cardiovascular diseases. Cardiovascular diseases (CVDs), such as ischaemic heart disease, cardiomyopathy, atherosclerosis, hypertension, stroke and heart failure, are among the leading causes of morbidity and mortality worldwide. Although specific CVDs and the associated cardiometabolic abnormalities have distinct pathophysiological and clinical manifestations, they often share common traits, including disruption of proteostasis resulting in accumulation of unfolded or misfolded proteins in the endoplasmic reticulum (ER). ER proteostasis is governed by the unfolded protein response (UPR), a signalling pathway that adjusts the protein-folding capacity of the cell to sustain the cell's secretory function. When the adaptive UPR fails to preserve ER homeostasis, a maladaptive or terminal UPR is engaged, leading to the disruption of ER integrity and to apoptosis. ER stress functions as a double-edged sword, with long-term ER stress resulting in cellular defects causing disturbed cardiovascular function. In this Review, we discuss the distinct roles of the UPR and ER stress response as both causes and consequences of CVD. We also summarize the latest advances in our understanding of the importance of the UPR and ER stress in the pathogenesis of CVD and discuss potential therapeutic strategies aimed at restoring ER proteostasis in CVDs.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据