The role of heat shock proteins (HSPs) in type 2 diabetes mellitus pathophysiology
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 mitocho...
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Published in | Journal of diabetes and its complications Vol. 37; no. 11; p. 108564 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
01.11.2023
Elsevier Limited |
Subjects | |
Online Access | Get full text |
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Summary: | 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.
•The altered expression of HSPs in T2DM holds great potential to investigate their role in disease pathogenesis and their applicability as a target in clinical approaches. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 ObjectType-Review-3 content type line 23 |
ISSN: | 1056-8727 1873-460X 1873-460X |
DOI: | 10.1016/j.jdiacomp.2023.108564 |