The alarmingly high global prevalence of Type 2 Diabetes Mellitus (T2DM) has made novel treatment strategies imperative. One major contributing factor to the onset of T2DM is mitochondrial dysfunction, which deteriorates cellular health, interferes with energy metabolism, and reduces insulin sensitivity. Targeting mitochondrial pathways can enhance outcomes in T2DM. Promising therapeutic benefits can be derived from strategies that target and improve mitochondrial function, biogenesis, efficient turnover, and oxidative stress reduction. Through increased mitochondrial efficiency and improved insulin action, these treatments seek to address the complex problems associated with T2DM. The complexities of mitochondrial dynamics, such as their role in energy production, appropriate regulation of cell death, and creation of reactive oxygen species (ROS), highlight the necessity of comprehensive approaches in the development of medicines that target the mitochondria. This strategy represents a step forward in the management of T2DM and highlights a promising area of cutting edge research in the hunt for potent treatments that might stop or reverse the disease's development, improving patient outcomes and care.
Key words: T2DM; Mitochondrial Dysfunction; Epigenetics; Insulin Resistance; Oxidative Stress
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