AI Article Synopsis
- Resident synoviocytes, immune cells, and synovial microvasculature work together to create pannus in rheumatoid arthritis (RA), leading to joint damage.
- These cells undergo a shift from using oxygen for energy to glycolysis due to a harsh environment characterized by low oxygen and nutrients, which boosts their growth.
- The review examines how this metabolic adaptation affects disease development and suggests potential new targets for anti-rheumatic therapies by analyzing the changes in proteins and enzymes related to glycolysis.
Article Abstract
Resident synoviocytes and synovial microvasculature, together with immune cells from circulation, contribute to pannus formation, the main pathological feature of rheumatoid arthritis (RA), leading to destruction of adjacent cartilage and bone. Seeds, fibroblast-like synoviocytes (FLSs), macrophages, dendritic cells (DCs), B cells, T cells and endothelial cells (ECs) seeds with high metabolic demands undergo metabolic reprogramming from oxidative phosphorylation to glycolysis in response to poor soil of RA synovium with hypoxia, nutrient deficiency and inflammatory stimuli. Glycolysis provides rapid energy supply and biosynthetic precursors to support pathogenic growth of these seeds. The metabolite lactate accumulated during this process in turn condition the soil microenvironment and affect seeds growth by modulating signalling pathways and directing lactylation modifications. This review explores in depth the survival mechanism of seeds with high metabolic demands in the poor soil of RA synovium, providing useful support for elucidating the etiology of RA. In addition, we discuss the role and major post-translational modifications of proteins and enzymes linked to glycolysis to inspire the discovery of novel anti-rheumatic targets.
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| http://dx.doi.org/10.1016/j.intimp.2024.111913 | DOI Listing |
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