Blood: NCOA4 mediates hepatic iron reserve mobilization after blood loss.

!----: The mobilization of the hepatic iron reserve after NCOA4 mediated blood loss, and the Expression of NCOA4 is increased by HIF-1 alpha/HIF-2 alpha-dependence in conditions that promote HIF stabilitysummary: The mechanism of releasing blood to promote the mobilization of hepatic iron reserves is not clearNCOA4 (nuclear receptor co-activation factor 4) is a widely expressed intracellular protein that has been shown to mediate the autophageline degradation of ferriteIn this study, Li and others studied the local demand of NCOA4 in regulating the liver iron reserves and the regulation mechanism of NCOA4in mice that did not release blood, the Ncoa4 gene, which targeted the removal of liver cells, had little effect on the level of ferritin subunits in the liver and the concentration of non-hemoglobin ironAfterblood letting go, mice that targeted mice that struck out the ncoa4 gene of the liver cell developed anemia and hypoferric, similar to those of Ncoa4-regulated controlled control mice, but the ability to reduce the level of liver ferritin subunits and the concentration of non-hemoglobin iron in the liver decreased significantlyliver reactions to this damage can be observed even with limited dietary ironin human and mouse liver cancer cell lines, stable hypoxic induction factors (HIF) chemicals, including tinmine, cobalt chloride and metraisey glycine, can improve the expression of NCOA4 mRNAthis induction of NCOA4 mRNA occurs within 3 hours, before the increase of the NCOA4 protein, and weakens in the case of double knockout of HIF-1a and HIF-2athe above, this study shows for the first time the role of NCOA4 in promoting the mobilization of liver iron after blood loss, as well as the expression of NCOA4 in HIF regulation of liver-derived cellsGiven that proline hydroxylase, which regulates HIF stability, is an oxygen and iron-dependent enzyme, this study suggests a new mechanism, namely, that hypoxia and iron deficiency may affect the internal balance of iron by regulating the expression of NCOA4.