Pathological mechanisms of abnormal iron metabolism and mitochondrial dysfunction in systemic lupus erythematosus

Introduction: Systemic lupus erythematosus [SLE] is a chronic, autoimmune condition characterized by the formation of autoantibodies directed against nuclear components and by oxidative stress. Recently, a number of studies have demonstrated the essential role of iron in the immune response and there is growing evidence that abnormal iron homeostasis can occur in the chronic inflammatory state seen in SLE. Not only is iron vital for hematopoiesis, it is also important for a number of other key physiological processes, in particular in maintaining healthy mitochondrial function. Areas covered: In this review, we highlight the latest understanding with regards to how patients with SLE may be at risk of cellular iron depletion as a result of both absolute and functional iron deficiency. Furthermore, we aim to explain the latest evidence of mitochondrial dysfunction in the pathogenesis of the disease. Expert opinion: Growing evidence suggests that both abnormal iron homeostasis and subsequent mitochondrial dysfunction can impair effector immune cell function. Through a greater understanding of these abnormalities, therapeutic options that directly target iron and mitochondria may ultimately represent novel treatment targets that may translate into clinical care of patients with SLE in the near future.