Delphine Meynard

TL;DR: It is shown that targeted disruption of Bmp6 in mice causes a rapid and massive accumulation of iron in the liver, the acinar cells of the exocrine pancreas, the heart and the renal convoluted tubules, and this indicates that BMP6 is critical for iron homeostasis and that it is functionally nonredundant with other members of the Bmp subfamily.

TL;DR: This study points out molecules that appear to play a critical role in the control of systemic iron balance, including Smad4, which is required for activation of Smad7, Id1, and Atoh8 transcription by iron, and 4 which are related to the BMP/Smad pathway.

TL;DR: It is demonstrated that both transferrin saturation and liver iron content independently influence hepcidin expression, whereas the hepatic Erk1/2 signaling pathway is not activated by iron in vivo.

TL;DR: How the liver is the central conductor of systemic iron balance is reviewed and shown that this central role is related to the secretion of a peptide hormone hepcidin by hepatocytes.

TL;DR: The inappropriately low levels of Id1 and hepcidin mRNA observed at weaning suggest that Hfe deficiency triggers iron overload by impairing hepatic Bmp/Smad signaling, and HFE appears to facilitate signal transduction induced by the BMP6 ligand.