Abnormal Mitochondrial Physiology in the Pathogenesis of Systemic Lupus Erythematosus

Abstract

Systemic lupus erythematosus (SLE) is an autoimmune disorder characterized by abnormalities within the innate and adaptive immune systems. Activation and proliferation of a wide array of immune cells require significant up-regulation in cellular energy metabolism, with the mitochondria playing an essential role in the initiation and maintenance of this response. This article highlights how abnormal mitochondrial function may occur in SLE and focuses on how energy metabolism, oxidative stress, and impaired mitochondrial repair play a role in the pathogenesis of the disease. How this may represent an appealing novel therapeutic target for future drug therapy in SLE also is discussed.

Keywords: Antimitochondrial antibodies; Autoimmunity; Immunometabolism; Mitochondria; Mitophagy; Reactive oxygen species; Systemic lupus erythematosus; T-cells.