posted on 2023-05-21, 03:39authored byMustapha, S, Mohammed, M, Azemi, AK, Jatau, AI, Shehu, A, Mustapha, L, Aliyu, IM, Danraka, RN, Amin, A, Bala, AA, Wan Ahmad, WAN, Rasool, AHG, Mustafa, MR, Mokhtar, SS
The endoplasmic reticulum (ER) plays a multifunctional role in lipid biosynthesis, calcium storage, protein folding, and processing. Thus, maintaining ER homeostasis is essential for cellular functions. Several pathophysiological conditions and pharmacological agents are known to disrupt ER homeostasis, thereby, causing ER stress. The cells react to ER stress by initiating an adaptive signaling process called the unfolded protein response (UPR). However, the ER initiates death signaling pathways when ER stress persists. ER stress is linked to several diseases, such as cancer, obesity, and diabetes. Thus, its regulation can provide possible therapeutic targets for these. Current evidence suggests that chronic hyperglycemia and hyperlipidemia linked to type II diabetes disrupt ER homeostasis, thereby, resulting in irreversible UPR activation and cell death. Despite progress in understanding the pathophysiology of the UPR and ER stress, to date, the mechanisms of ER stress in relation to type II diabetes remain unclear. This review provides up-to-date information regarding the UPR, ER stress mechanisms, insulin dysfunction, oxidative stress, and the therapeutic potential of targeting specific ER stress pathways.
History
Publication title
Molecules
Volume
26
Issue
14
Pagination
1-16
ISSN
1420-3049
Department/School
School of Pharmacy and Pharmacology
Publisher
Molecular Diversity Preservation International
Place of publication
Matthaeusstrasse 11, Basel, Switzerland, Ch-4057
Rights statement
Copyright 2021 the authors. Licensed under Creative Commons Attribution 4.0 International (CC BY 4.0) https://creativecommons.org/licenses/by/4.0/