Abnormal energy metabolism in the pathogenesis of systemic lupus erythematosus

Systemic lupus erythematosus (SLE) is a severe autoimmune disease with significant socioeconomic impact worldwide. Orderly energy metabolism is essential for normal immune function, and disordered energy metabolism is increasingly recognized as an important contributor to the pathogenesis of SLE. Disorders of energy metabolism are characterized by increased reactive oxygen species, ATP deficiency, and abnormal metabolic pathways. Oxygen and mitochondria are critical for the production of ATP, and both mitochondrial dysfunction and hypoxia affect the energy production processes. In addition, several signaling pathways, including mammalian target of rapamycin (mTOR)/adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) signaling and the hypoxia-inducible factor (HIF) pathway also play important regulatory roles in energy metabolism. Furthermore, drugs with clear clinical effects on SLE, such as sirolimus, metformin, and tacrolimus, have been proven to improve the disordered energy metabolism of immune cells, suggesting the potential of targeting energy metabolism for the treatment of SLE. Moreover, several metabolic modulators under investigation are expected to have potential therapeutic effects in SLE. This review aimed to gain insights into the role and mechanism of abnormal energy metabolism in the pathogenesis of SLE, and summarizes the progression of metabolic modulator in the treatment of SLE.