Metabolism as a key regulator in the pathogenesis of systemic lupus erythematosus

In the middle of the 20th century, biologists focused on investigating the mechanism of gene regulation and signal transduction in cells, which led to the concept that metabolites were products of gene expression and signal transduction pathways. In the 1920s, the importance of cellular metabolism was shown in the Warburg effect, in which cancer cells are characterized by a mitochondrial defect that shifts towards aerobic glycolysis. Recently, it is accepted that each organ and cell subset needs specific metabolic conditions and metabolic regulatory systems. Immunometabolism is a relatively new field of metabolism studies. The immune system consists of various cell subsets that have unique requirements and functions. The metabolic reprogramming in each immune cell causes different effects on different cell subsets. For example, resting lymphocytes generate energy through oxidative phosphorylation (OXPHOS) and fatty acid oxidation (FAO), whereas activated lymphocytes rapidly shift to the glycolytic pathway. A detailed understanding of metabolic regulation has progressed rapidly, especially in T cells during their differentiation from naïve to effector T cells. Metabolism is now considered to play a key role in autoimmune diseases. Metabolic changes in autoimmune diseases might be due to inflammation as well as being involved in autoimmune pathogenesis. Systemic lupus erythematosus (SLE) is an autoimmune disease with heterogenous clinical presentations whose precise pathophysiological mechanism is largely unknown. In this report, we review the altered metabolism in SLE and discuss the potential of metabolomics for accelerating the discovery of novel cellular autoimmune therapies and novel disease biomarkers.