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ER Stress in Cardiometabolic Diseases: From Molecular Mechanisms to Therapeuticsстатья
Статья опубликована в высокорейтинговом журнале
Статья опубликована в журнале из списка Web of Science и/или Scopus- Авторы: Ajoolabady A., Wang S., Kroemer G., Klionsky D.J., Uversky V.N., Sowers J.R., Aslkhodapasandhokmabad H., Bi Y., Ge J., Ren J.
- Журнал: Endocrine Reviews
- Том: 42
- Номер: 6
- Год издания: 2021
- Издательство: The Endocrine Society
- Местоположение издательства: United States
- Первая страница: 839
- Последняя страница: 871
- Аннотация: 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.
- Добавил в систему: Уверский Владимир Николаевич