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Autoantibody production in SLE is believed to be triggered by molecular mimicry, abnormal antigen presentation, and modification of endogenous antigens, which lead to the formation of pathogenic immune complexes that deposit in tissues and drive inflammation [89]

doi: 10.1007/s13760-016-0697-z 165

The ppar/activator gw 501516 prevents the down-regulation of ampk caused by a high-fat diet in liver and amplifies the pgc-1-lipin 1-ppar pathway leading to increased fatty acid oxidation

This mechanism has been confirmed in both mouse models and human lymphoma, and demethylating drugs (e.g., 5-aza-2'-deoxycytidine) can restore Spry2 expression and suppress ERK activity (Frank et al., 2009[32])

Proline and glycinebetaine ameliorated NaCl stress via scavenging of hydrogen peroxide and methylglyoxal but not superoxide or nitric oxide in tobacco cultured cells