ILLUMINATING THE ER-DIABETES RELATIONSHIP: THE HIDDEN CATALYST IN DIABETES DEVELOPMENT AND PROGRESSION

Abstract

Endoplasmic reticulum (ER) stress has emerged as a critical factor in the development and progression of diabetes, encompassing both type 1 diabetes (T1D) and type 2 diabetes (T2D). The ER plays a pivotal role in protein folding, lipid synthesis, and calcium homeostasis. However, when the ER is subjected to stress, it activates the unfolded protein response (UPR) to restore homeostasis. Prolonged ER stress and chronic UPR activation have been implicated in pancreatic β-cell dysfunction, insulin resistance, and inflammation, all of which are hallmarks of diabetes.Recent studies have highlighted the complex interplay between ER stress, oxidative stress, and inflammatory pathways in the pathogenesis of T1D and T2D. Furthermore, research has shown that targeting ER stress and the UPR may offer novel therapeutic strategies for the treatment and prevention of diabetes. This review aims to provide a comprehensive overview of the current understanding of ER stress in diabetes, including its molecular mechanisms, cellular consequences, and potential therapeutic interventions. By synthesizing findings from recent studies, this review seeks to contribute to the development of innovative treatments for diabetes and to shed light on the intricate relationships between ER stress, β-cell function, and glucose metabolism.

DOI - https://doi.org/10.65525/SVUP.9788198800473.2025.395-417