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

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.