This review innovatively summarizes the distinct characteristics of glucose metabolism reprogramming in multiple immune and stromal cells during RA progression, and systematically elucidates the regulatory mechanisms by which hypoxic microenvironments, lactate metabolism, and lactylation trigger glucose metabolic dysregulation.
Abstract
Rheumatoid arthritis (RA) is a prevalent autoimmune disease characterized primarily by chronic inflammation of the synovial membrane and destruction of articular cartilage and bone. Previous research has predominantly focused on the abnormal activation of immune cells and the cascade of inflammatory cytokines. However, recent studies have reported that energy metabolism disorders, particularly glucose metabolism reprogramming, are closely associated with the pathogenesis of RA. Hypoxia, lactate production, and lactate modification within the synovial microenvironment are closely associated with glucose metabolism reprogramming. This reprogramming supports the elevated energy and nutrient requirement for abnormal immune cell activation and effector cell proliferation, thereby serving as a core event in RA pathogenesis. Traditional Chinese medicine (TCM) that modulates regulatory factors or pathological products related to glucose metabolism reprogramming in RA represents a promising therapeutic strategy for regulating immune responses and delaying disease progression. This review innovatively summarizes the distinct characteristics of glucose metabolism reprogramming in multiple immune and stromal cells (including fibroblast-like synoviocytes, macrophages, B cells, vascular endothelial cells and T cells) during RA progression, and systematically elucidates the regulatory mechanisms by which hypoxic microenvironments, lactate metabolism, and lactylation trigger glucose metabolic dysregulation. Furthermore, we provide a comprehensive and cutting-edge overview of the targeted modulatory effects of TCM monomers, active ingredients, and compound formulas on glucose metabolism reprogramming and lactylation in RA. Graphical Abstract
Abstract Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by persistent synovitis and progressive structural joint damage. Its pathology involves immune-cell infiltration, pannus formation, cartilage degradation, and bone destruction. Although autoantibodies, inflammatory cytokines, and aberrant...
Ting-Ting Li, Guang-Huan Li, Yu-Yao Yang et al.· Journal of Inflammation Rese...· 0 citations
This review systematically consolidates current mechanistic understanding and critically assesses translational gaps, including the predominance of rodent collagen-induced arthritis models, the scarcity of human synovial macrophage validation, undefined pharmacokinetics of active metabolites, and the need for patient s...
Wen-Jiao Wang, Jian-Hui Ma, Xu-Dong Zhang et al.· Frontiers in Pharmacology· 0 citations
This review summarizes current findings on major common metabolic dysregulation in cancer and SLE, highlighting the interplay of metabolic disturbances, mitochondrial dysfunction and disease pathogenesis and explores the potential of targeting metabolic pathways as a therapeutic strategy to mitigate organ damage and im...
Jaron Dalgleish, Maurice Tohme, Michael D. Pisano et al.· Biomolecules· 0 citations
This review examines metabolism–inflammation crosstalk in cardiovascular disease by linking core inflammatory pathways with metabolic sensors, immune-cell metabolic reprogramming and signaling metabolites, then comparing disease-specific mechanisms in myocardial infarction/ischemia–reperfusion injury, heart failure, at...
Rheumatoid arthritis (RA) is a systemic autoimmune disease marked by chronic inflammation and destruction of joints and surrounding soft tissues. The pathogenesis of RA is heavily driven by two intertwined and mutually regulatory processes: metabolic reprogramming and epigenetic remodeling. Recent advances reveal a cru...
Zhi-Qiang Luo, Shunqian Yao, Zhuquan Zhu et al.· Frontiers in Pharmacology· 0 citations
How changes in glucose, lipid, and mitochondrial metabolism influence immune responses that lead to chronic inflammation and autoimmunity in MS, RA, and T1D is discussed.
Andisheh Mosaffa Jahromi, Fatemeh Mirzaei, Sara Mirzazadeh et al.· Cellular & Molecular Immunol...· 0 citations
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