Mitochondria dysfunction: A trigger for cardiovascular diseases in systemic lupus erythematosus

[Display omitted] •Mitochondrial dysfunction plays a key role in cardiovascular disease in SLE patients.•Oxidative stress and immune dysregulation drive cardiovascular complications in SLE.•Therapeutic strategies targeting mitochondria may improve SLE cardiovascular outcomes.•Antioxidants and AMPK activators hold promise for mitigating SLE-related heart disease.•This review identifies new therapeutic targets to address SLE-related cardiovascular risk. Cardiovascular disease (CVD), including pericarditis, myocarditis, sudden cardiac death, coronary heart disease, and stroke, are leading contributors to morbidity and mortality in systemic lupus erythematosus (SLE) patients. Emerging evidence highlights mitochondrial dysfunction as a key driver of cardiovascular pathology in SLE, with impaired oxidative phosphorylation, altered membrane potential, and disrupted metabolic processes promoting oxidative stress, inflammatory activation, and endothelial dysfunction. This review critically examines mitochondrial contributions to CVD in SLE, comparing these mechanisms with those in non-SLE CVD to highlight SLE-specific mitochondrial vulnerabilities. Furthermore, we discuss preclinical and clinical findings supporting mitochondrial pathways as potential therapeutic targets, aiming to bridge gaps in current understanding and outline future research directions. By synthesizing current knowledge of mitochondrial dysregulation, this review proposes therapeutic strategies to improve cardiovascular outcomes and advance patient care in SLE.