Systemic Lupus Erythematosus (SLE) is a chronic immune-mediated inflammatory disease characterized by dysregulated immune tolerance, abnormal secretion of autoantibodies, and multi-organ damage. Among them, mutations in genetic susceptibility genes, abnormal epigenetic modifications, excessive oxidative stress, abnormal accumulation of inflammatory factors, and intestinal flora disorders are all key specific factors that lead to immune dysfunction, abnormal production of autoantibodies, and multi-organ damage in patients with SLE. The bone marrow microenvironment, as a key niche for immune cell development, plays a pivotal role in the pathogenesis of SLE, especially through the metabolic reprogramming of bone marrow mesenchymal stromal cells (BMSCs). Recently, studies have demonstrated that under the influence of the bone marrow microenvironment, BMSCs can undergo metabolic reprogramming, regulated by the aforementioned abnormal factors related to SLE, the key metabolic pathways such as glucose metabolism, lipid metabolism and mitochondrial metabolism are disrupted, thereby affecting their regulatory functions on various immune cells. This process plays a role in the development and progression of immune-mediated inflammatory diseases like SLE. This article provides a comprehensive review of the current knowledge regarding the metabolic regulatory mechanism of the BMSCs on the immune cells in SLE and discusses recent advances in clinical translation.
Yang et al. (Fri,) studied this question.