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Endoplasmic reticulum stress and unfolded protein response in cardiovascular diseases

Nature reviews cardiology, 2021-07, Vol.18 (7), p.499-521 [Peer Reviewed Journal]

COPYRIGHT 2021 Nature Publishing Group ;Springer Nature Limited 2021. ;ISSN: 1759-5002 ;EISSN: 1759-5010 ;DOI: 10.1038/s41569-021-00511-w ;PMID: 33619348

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  • Title:
    Endoplasmic reticulum stress and unfolded protein response in cardiovascular diseases
  • Author: Ren, Jun ; Bi, Yaguang ; Sowers, James R ; Hetz, Claudio ; Zhang, Yingmei
  • Subjects: Biological control systems ; Cardiovascular diseases ; Cardiovascular Diseases - physiopathology ; Cardiovascular research ; Development and progression ; Endoplasmic reticulum ; Endoplasmic Reticulum Stress - physiology ; Health aspects ; Humans ; Pathogenesis ; Physiological aspects ; Protein folding ; Proteins ; Stress (Physiology) ; Unfolded Protein Response - physiology
  • Is Part Of: Nature reviews cardiology, 2021-07, Vol.18 (7), p.499-521
  • Description: 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.
  • Publisher: England: Nature Publishing Group
  • Language: English
  • Identifier: ISSN: 1759-5002
    EISSN: 1759-5010
    DOI: 10.1038/s41569-021-00511-w
    PMID: 33619348
  • Source: MEDLINE
    ProQuest Central
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