Author & Research Contributor
Published in 2026 | VOLUME 03, SEPTEMBER ISSUE 09Type 2 diabetes mellitus has become one of the fastest-growing global health crises, affecting millions worldwide. This review explores the intricate relationship between mitochondrial dysfunction and oxidative stress in driving the development and progression of this metabolic disorder. Chronic high blood sugar levels trigger excessive production of reactive oxygen species from dysfunctional mitochondria, creating a destructive cycle that impairs insulin action, damages insulin-producing pancreatic cells, and fuels persistent low-grade inflammation. These interconnected pathological processes ultimately lead to the metabolic breakdown characteristic of type 2 diabetes. The review also examines emerging therapeutic strategies, including mitochondria-targeted antioxidants and lifestyle interventions that show promise in restoring cellular energy balance and breaking this harmful cycle.
Type 2 diabetes mellitus; oxidative stress; mitochondrial dysfunction; reactive oxygen species (ROS); insulin resistance; pancreatic ?-cell failure; electron transport chain (ETC); glucolipotoxicity; mitochondrial dynamics (fusion/fission); mitophagy; mitochondrial biogenesis; PGC-1?; antioxidant defense systems (SOD, CAT, GPx); NLRP3 inflammasome; chronic low-grade inflammation; stress kinases (JNK, NF-?B); insulin signaling (IRS-1/PI3K/Akt); ER stress; unfolded protein response; mitochondria-targeted antioxidants (MitoQ, SkQ1, MitoTEMPO); AMPK activators; SGLT2 inhibitors; metformin; lifestyle interventions; metabolic syndrome.