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. 2021 Mar 26;5(5):723–735. doi: 10.1002/hep4.1717

FIG. 3.

FIG. 3

Increased hepcidin production in response to inflammation (adapted from Camaschella et al.( 2 )). The current evidence suggests that inflammation influences hepcidin expression primarily through the JAK‐STAT pathway. Increased LPS produced in the setting of infection or inflammation increases production of IL‐6 in macrophages through TLR4 binding. IL‐6 then binds to its receptor on hepatocytes and may bind directly to hepatocytes, resulting in activation of the JAK2‐STAT3 signaling pathway through phosphorylation of STAT3; phosphorylated STAT3 then enters the nucleus and increases hepcidin transcription by binding to the STAT3 responsive element on the hepcidin promoter. LPS‐activated myeloid differentiation protein 88 in hepatocytes may also increase SMAD signaling through SMAD4. In addition, it has been proposed from observations in animals that cross‐talk between BMP and STAT3 may also contribute to hepcidin expression. Abbreviations: BRE, BMP responsive element; FPN, ferroportin; MYD888, myeloid differentiation protein 88; SRE, STAT3 responsive element.