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While Keap-1 acts as the inhibitor of Nrf-2 and controls its stability

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Emerging therapeutic strategies for SLE extend beyond B cell depletion to target CD4 follicular helper T (Tfh) cells: E4BP4 inhibits Tfh differentiation by repressing BCL-6 transcription via recruitment of HDAC1 and EZH2, while impaired E4BP4 function and IFN-Idriven IL-21/IFN- production promote Tfh expansion and autoreactive B cell responses, supporting Tfh-directed CAR-T approaches (54, 55)

Persistent ferroptosis in alveolar and endothelial cells triggers pro-fibrotic signaling pathways, such as those involving TGF- and connective tissue growth factor (CTGF), which drive ECM deposition and fibroproliferation