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Chronic hyperglycemia, lipotoxicity, and inflammation impair mitochondrial quality control (MQC), leading to \u03b2 cell dysfunction, oxidative stress, and apoptosis. Mitochondria\u2010organelle interactions, particularly with the endoplasmic reticulum (ER), lysosomes, and Golgi apparatus, further exacerbate \u03b2 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 \u03b2 cell function. However, clinical validation is needed. 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