Endoplasmic reticulum stress in diseases.
diseases
endoplasmic reticulum stress (ER stress)
therapeutic strategies
unfolded protein response (UPR)
Journal
MedComm
ISSN: 2688-2663
Titre abrégé: MedComm (2020)
Pays: China
ID NLM: 101769925
Informations de publication
Date de publication:
Sep 2024
Sep 2024
Historique:
received:
21
02
2023
revised:
30
07
2024
accepted:
31
07
2024
medline:
27
8
2024
pubmed:
27
8
2024
entrez:
27
8
2024
Statut:
epublish
Résumé
The endoplasmic reticulum (ER) is a key organelle in eukaryotic cells, responsible for a wide range of vital functions, including the modification, folding, and trafficking of proteins, as well as the biosynthesis of lipids and the maintenance of intracellular calcium homeostasis. A variety of factors can disrupt the function of the ER, leading to the aggregation of unfolded and misfolded proteins within its confines and the induction of ER stress. A conserved cascade of signaling events known as the unfolded protein response (UPR) has evolved to relieve the burden within the ER and restore ER homeostasis. However, these processes can culminate in cell death while ER stress is sustained over an extended period and at elevated levels. This review summarizes the potential role of ER stress and the UPR in determining cell fate and function in various diseases, including cardiovascular diseases, neurodegenerative diseases, metabolic diseases, autoimmune diseases, fibrotic diseases, viral infections, and cancer. It also puts forward that the manipulation of this intricate signaling pathway may represent a novel target for drug discovery and innovative therapeutic strategies in the context of human diseases.
Identifiants
pubmed: 39188936
doi: 10.1002/mco2.701
pii: MCO2701
pmc: PMC11345536
doi:
Types de publication
Journal Article
Review
Langues
eng
Pagination
e701Informations de copyright
© 2024 The Author(s). MedComm published by Sichuan International Medical Exchange & Promotion Association (SCIMEA) and John Wiley & Sons Australia, Ltd.
Déclaration de conflit d'intérêts
The authors declare no conflict of interest.