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Anti-GAPDH autoantibody is associated with increased disease activity and intracranial pressure in systemic lupus erythematosus

It then inhibits adipocyte lipolysis and increases FFAs in cells, further stimulating the LDLs accumulation and secretion, inducing lipid metabolism disorders, lipotoxicity, and even cell necrosis, finally resulting in diabetic myocardial damage

With the primary condition, not enough carnitine can get into cells because of a genetic problem

This finding aligns with the role of fatty acid metabolism in promoting T cell memory, highlighting a critical role of TCA cycle direction and metabolism in T cell fate decisions