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Hydroxychloroquine is a classical therapeutic agent for RA, and its therapeutic mechanism is related to the inhibition of dendritic cell (DC) activation by blocking TLR9 activation (169)

By inactivating ERK signaling, silencing of aldoketo reductase family 1 member C3 (AKR1C3) is reported to inhibit autophagy-dependent glycolysis in TC [273]

Many studies have identified a proximal AP-1 element (263 to 269) to be critical in mediating the effect of oxidative stress-induced increase in human GCLC transcription (Morales et al., 1997

Sacks D, Baxter B, Campbell BC, Carpenter JS, Cognard C, Dippel D, Eesa M, Fischer U, Hausegger K, Hirsch JA (2018) Multisociety consensus quality improvement revised consensus statement for endovascular therapy of acute ischemic stroke

S., Chang, H., Salzmann, S., Muller, C