ER Stress in Cardiometabolic Diseases: From Molecular Mechanisms to Therapeutics
Document Type
Article
Publication Date
2021
Digital Object Identifier (DOI)
https://doi.org/10.1210/endrev/bnab006
Abstract
The endoplasmic reticulum (ER) hosts linear polypeptides and fosters natural folding of proteins through ER-residing chaperones and enzymes. Failure of the ER to align and compose proper protein architecture leads to accumulation of misfolded/unfolded proteins in the ER lumen, which disturbs ER homeostasis to provoke ER stress. Presence of ER stress initiates the cytoprotective unfolded protein response (UPR) to restore ER homeostasis or instigates a rather maladaptive UPR to promote cell death. Although a wide array of cellular processes such as persistent autophagy, dysregulated mitophagy, and secretion of proinflammatory cytokines may contribute to the onset and progression of cardiometabolic diseases, it is well perceived that ER stress also evokes the onset and development of cardiometabolic diseases, particularly cardiovascular diseases (CVDs), diabetes mellitus, obesity, and chronic kidney disease (CKD). Meanwhile, these pathological conditions further aggravate ER stress, creating a rather vicious cycle. Here in this review, we aimed at summarizing and updating the available information on ER stress in CVDs, diabetes mellitus, obesity, and CKD, hoping to offer novel insights for the management of these cardiometabolic comorbidities through regulation of ER stress.
Was this content written or created while at USF?
Yes
Citation / Publisher Attribution
Endocrine Reviews, v. 42, issue 6, p. 839-871
Scholar Commons Citation
Ajoolabady, Amir; Wang, Shuyi; Kroemer, Guido; Klionsky, Daniel J.; Uversky, Vladimir N.; Sowers, James R.; Aslkhodapasandhokmabad, Hamid; Bi, Yaguang Bi; Ge, Junbo; and Ren, Jun, "ER Stress in Cardiometabolic Diseases: From Molecular Mechanisms to Therapeutics" (2021). Molecular Medicine Faculty Publications. 997.
https://digitalcommons.usf.edu/mme_facpub/997
