Journal of Diabetes · Published 2026-04-29 · DOI 10.1111/1753-0407.70228
ABSTRACT Mitochondrial homeostasis is essential for pancreatic β cell function, and its disruption underlies diabetes pathogenesis. Chronic hyperglycemia, lipotoxicity, and inflammation impair mitochondrial quality control (MQC), leading to β cell dysfunction, oxidative stress, and apoptosis. Mitochondria‐organelle interactions, particularly with the endoplasmic reticulum (ER), lysosomes, and Golgi apparatus, further exacerbate β cell dysfunction by disrupting calcium signaling and metabolic coordination. Emerging potential therapies, such as DRAK2 inhibitors and metabolic reprogramming agents, show promise in preserving MQC and β cell function. However, clinical validation is needed. This review highlights mitochondrial dysfunction as a central driver of diabetes and underscores the potential of mitochondrial‐targeted strategies for therapeutic intervention.
Abstract from DOAJ. Public domain (CC0 1.0).
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