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editorial
. 2021 Nov 26;13(5):313–315. doi: 10.1007/s13238-021-00892-1

Figure 1.

Figure 1

Neutrophil ferroptosis promote SLE pathogenesis. INFα and IgG in SLE serum activate the CaMKIV-CREMα axis, enhance the binding of CREMα to GPX4 promoter, suppress GPX4 expression, followed by increase lipid peroxidation levels. These lead to neutrophil ferroptosis and promote SLE pathogenesis. SLE: systemic lupus erythematosus; IFN-α: interferon-α; IgG: immunoglobulin G; CaMKIV: calcium/calmodulin kinase IV; CREMα: cAMP-responsive element modulator α; GPX4: glutathione peroxidase 4; GSH: glutathione; GSSH: oxidized glutathione