Mitochondrial Dysfunction in Diabetic Cardiomyopathy: New Therapeutic Targets

Background: To evaluate the effects of a mitochondria-targeted therapeutic intervention on mitochondrial bioenergetics, oxidative stress, and cardiac function in patients with DCM. Methods: This prospective, comparative study enrolled 71 patients with echocardiographically confirmed DCM between March 2023 and March 2024. Participants were assigned to either standard therapy (n=36) or standard therapy plus a mitochondria-targeted agent (n=35). Baseline and six-month follow-up assessments included echocardiographic parameters, NT-proBNP levels, HbA1c, lipid profile, oxidative stress markers, and mitochondrial function measures in peripheral blood mononuclear cells (ATP production, ROS levels, respiratory chain complex I and IV activity, and mitochondrial DNA copy number). Results: Compared with the standard therapy group, the intervention group demonstrated significantly higher ATP production (p<0.001), increased complex I (p<0.001) and complex IV activity (p=0.002), and lower ROS levels (p<0.001). LVEF improved modestly (p=0.03), while NT-proBNP levels declined (p=0.01). HbA1c decreased slightly but significantly (p=0.03), and malondialdehyde levels were markedly reduced (p<0.001). No major adverse events were reported. Conclusion: Mitochondria-targeted therapy improved mitochondrial function, reduced oxidative stress, and enhanced selected cardiac performance indices in DCM patients. These findings support the therapeutic potential of targeting mitochondrial pathways alongside conventional management.