The role of heat shock proteins (HSPs) in type 2 diabetes mellitus pathophysiology.

Autor: Esmaeilzadeh A; Department of Immunology, Zanjan University of Medical Sciences, Zanjan, Iran; Cancer Gene Therapy Research Center (CGRC), Zanjan University of Medical Sciences, Zanjan, Iran. Electronic address: A46reza@zums.ac.ir., Mohammadi V; School of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran., Elahi R; School of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran., Rezakhani N; School of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran.
Jazyk: angličtina
Zdroj: Journal of diabetes and its complications [J Diabetes Complications] 2023 Nov; Vol. 37 (11), pp. 108564. Date of Electronic Publication: 2023 Jul 23.
DOI: 10.1016/j.jdiacomp.2023.108564
Abstrakt: Type 2 diabetes mellitus (T2DM) is a metabolic disorder characterized by sustained hyperglycemia caused by impaired insulin signaling and secretion. Metabolic stress, caused by an inappropriate diet, is one of the major hallmarks provoking inflammation, endoplasmic reticulum (ER) stress, and mitochondrial dysfunction. Heat shock proteins (HSPs) are a group of highly conserved proteins that have a crucial role in chaperoning damaged and misfolded proteins to avoid disruption of cellular homeostasis under stress conditions. To do this, HSPs interact with diverse intra-and extracellular pathways among which are the insulin signaling, insulin secretion, and apoptosis pathways. Therefore, HSP dysfunction, e.g. HSP70, may lead to disruption of the pathways responsible for insulin secretion and uptake. Consistently, the altered expression of other HSPs and genetic polymorphisms in HSP-producing genes in diabetic subjects has made HSPs hot research in T2DM. This paper provides a comprehensive overview of the role of different HSPs in T2DM pathogenesis, affected cellular pathways, and the potential therapeutic strategies targeting HSPs in T2DM.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2023. Published by Elsevier Inc.)
Databáze: MEDLINE
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