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195,196,197 At the cellular level, this translates into a massive increase in cytoplasmic Na + concentration, membrane depolarisation and opening of voltage-gated Ca 2+ channels, which in turn promotes massive release of glutamate that results in even large depolarisation enlarging Na + and Ca 2+ influx thus completing the vicious circle of excitotoxic damage, as Ca 2+ overload triggers necrotic cell death
TNF- can downregulate adipocyte GLUT4 by Inhibit insulin receptor substrate1 (IRS-1) phosphorylation, increase free fatty acid (FFA) levels by 2-3-fold, and activate TLR4/NF-B pathway in FLS to promote the secretion of Matrix Metallopeptidase 3 (MMP-3), thus accelerating cartilage degradation ( HMGCR / LDLR ) through the nuclear translocation of SCAP-SREBP2, and enhance glycolytic enzyme expression via mTORC1, thereby resulting in a metabolic amplification effect ( miR-21, highly expressed in macrophages, can cause the accumulation of glycolytic intermediates by inhibiting PFK-M, activate DGAT to promote TG synthesis, and hinder FAO through the PTEN/PI3K/Akt pathway, thus creating a metabolic brake effect ( 4.2 Critical nodes of glycolipid metabolism regulation in RA The co-regulation of glycolipid metabolism in RA relies on the interaction among metabotropic nuclear receptors (PPAR/LXR), energy sensors (AMPK), and cholesterol synthesis axis (SCAP-SREBP)
