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Type 2 diabetes mellitus (T2DM) is a globally prevalent metabolic disorder characterized by insulin resistance and dysfunction of islet cells. Endoplasmic reticulum (ER) stress plays a crucial role in the pathogenesis and progression of T2DM, especially in the function and survival of β-cells. β-cells are particularly sensitive to ER stress because they require substantial insulin synthesis and secretion energy. In the early stages of T2DM, the increased demand for insulin exacerbates β-cell ER stress. Although the unfolded protein response (UPR) can temporarily alleviate this stress, prolonged or excessive stress leads to pancreatic cell dysfunction and apoptosis, resulting in insufficient insulin secretion. This review explores the mechanisms of ER stress in T2DM, particularly its impact on islet cells. We discuss how ER stress activates UPR signaling pathways to regulate protein folding and degradation, but when stress becomes excessive, these pathways may contribute to β-cell death. A deeper understanding of how ER stress impacts islet cells could lead to the development of novel T2DM treatment strategies aimed at improving islet function and slowing disease progression.
He et al. (Fri,) studied this question.