Ablation of Hepatocyte Smad1, Smad5, and Smad8 Causes Severe Tissue Iron Loading and Liver Fibrosis in Mice
Chia‐Yu Wang, Xia Xiao, Abraham Bayer, Yang Xu, Som Dev, Susanna Canali, Anil V. Nair, Ricard Masia, Jodie L. Babitt – 24 May 2019 – A failure of iron to appropriately regulate liver hepcidin production is central to the pathogenesis of hereditary hemochromatosis. SMAD1/5 transcription factors, activated by bone morphogenetic protein (BMP) signaling, are major regulators of hepcidin production in response to iron; however, the role of SMAD8 and the contribution of SMADs to hepcidin production by other systemic cues remain uncertain.