Publications

Mitochondrial dysfunction has emerged as a central mechanism linking metabolic derangements, immune dysregulation, and multi-organ toxicity in Type 2 Diabetes Mellitus (T2DM). Beyond its classical features of insulin resistance and hyperglycaemia, T2DM is characterized by impaired mitochondrial oxidative phosphorylation, altered mitochondrial dynamics, defective mitophagy, and excessive reactive oxygen species (ROS) production. These disturbances compromise cellular energy homeostasis and propagate oxidative stress, triggering inflammatory pathways and the release of mitochondrial damage-associated molecular patterns (DAMPs), which impair immune cell function. Dysfunctional mitochondria in metabolic tissues like skeletal muscle, liver, pancreas, and adipose tissue contribute directly to insulin resistance and β-cell failure, while in immune cells, they reduce regenerative capacity, promote apoptosis, and impair pathogen responses. Organ-specific consequences include hepatic steatosis, diabetic nephropathy, cardiomyopathy, skeletal muscle dysfunction, and cognitive decline. Additionally, extracellular vesicle-mediated transfer of dysfunctional mitochondria may amplify systemic inflammation and multi-organ stress. Therapeutic strategies targeting mitochondrial health, including mitochondria-specific antioxidants, modulators of mitochondrial dynamics, and enhancers of mitophagy and biogenesis, hold promise for mitigating both metabolic and immune dysfunction. Understanding mitochondrial impairment as a unifying mechanism in T2DM provides a framework for integrative interventions aimed at improving energy metabolism, immune competence, and organ resilience, potentially reducing disease progression and complications.