Systemic lupus erythematosus (SLE) is a complex, heterogeneous, systemic autoimmune disease involving a wide array of aberrant innate and adaptive immune responses. The immune microenvironment of SLE promotes the metabolic reprogramming of immune cells, leading to immune dyshomeostasis and triggering autoimmune inflammation. Different immune subsets switch from a resting state to a highly metabolic active state by alternating the redox-sensitive signaling pathway and the involved metabolic intermediates to amplify the inflammatory response, which is critical in SLE pathogenesis. In this review, we discuss abnormal metabolic changes in glucose metabolism, tricarboxylic acid cycle, and lipid and amino acid metabolism as well as mitochondrial dysfunction in immune cells in SLE. We also review studies focused on the potential targets for key molecules of metabolic pathways in SLE, such as hypoxia-inducible factor-1α, mammalian target of rapamycin, and AMP-activated protein kinase. We highlight the therapeutic rationale for targeting these pathways in treating SLE and summarize their recent clinical applications in SLE.
Keywords: Autoimmune disease; Metabolic reprogramming; Metabolism; Systemic lupus erythematosus (SLE).
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