Heat shock response during the resolution of inflammation and its progressive suppression in chronic-degenerative inflammatory diseases.
Chronic inflammatory diseases
Exercise
HSP70
Heat shock response
Insulin resistance
Obesity
Journal
Cell stress & chaperones
ISSN: 1466-1268
Titre abrégé: Cell Stress Chaperones
Pays: Netherlands
ID NLM: 9610925
Informations de publication
Date de publication:
Feb 2024
Feb 2024
Historique:
received:
18
09
2023
revised:
11
01
2024
accepted:
12
01
2024
medline:
6
3
2024
pubmed:
21
1
2024
entrez:
20
1
2024
Statut:
ppublish
Résumé
The heat shock response (HSR) is a crucial biochemical pathway that orchestrates the resolution of inflammation, primarily under proteotoxic stress conditions. This process hinges on the upregulation of heat shock proteins (HSPs) and other chaperones, notably the 70 kDa family of heat shock proteins, under the command of the heat shock transcription factor-1. However, in the context of chronic degenerative disorders characterized by persistent low-grade inflammation (such as insulin resistance, obesity, type 2 diabetes, nonalcoholic fatty liver disease, and cardiovascular diseases) a gradual suppression of the HSR does occur. This work delves into the mechanisms behind this phenomenon. It explores how the Western diet and sedentary lifestyle, culminating in the endoplasmic reticulum stress within adipose tissue cells, trigger a cascade of events. This cascade includes the unfolded protein response and activation of the NOD-like receptor pyrin domain-containing protein-3 inflammasome, leading to the emergence of the senescence-associated secretory phenotype and the propagation of inflammation throughout the body. Notably, the activation of the NOD-like receptor pyrin domain-containing protein-3 inflammasome not only fuels inflammation but also sabotages the HSR by degrading human antigen R, a crucial mRNA-binding protein responsible for maintaining heat shock transcription factor-1 mRNA expression and stability on heat shock gene promoters. This paper underscores the imperative need to comprehend how chronic inflammation stifles the HSR and the clinical significance of evaluating the HSR using cost-effective and accessible tools. Such understanding is pivotal in the development of innovative strategies aimed at the prevention and treatment of these chronic inflammatory ailments, which continue to take a heavy toll on global health and well-being.
Identifiants
pubmed: 38244765
pii: S1355-8145(24)00042-7
doi: 10.1016/j.cstres.2024.01.002
pii:
doi:
Substances chimiques
Heat Shock Transcription Factors
0
Inflammasomes
0
Heat-Shock Proteins
0
RNA, Messenger
0
NLR Proteins
0
HSP70 Heat-Shock Proteins
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
116-142Informations de copyright
Copyright © 2024. Published by Elsevier Inc.
Déclaration de conflit d'intérêts
Declarations of interest The authors declare no conflict of interest and no competing interests such as consultancies, financial involvement, patent ownership, etc. in relation to the work described. CNPq, FAPERGS, and CAPES (the funding organisms) had no involvement in the propositions presented in this manuscript.
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