Iron turns to wild when the transferrin is away

Abstract

In this issue of Blood, Yu et al report that hepatic transferrin (Trf) has a pivotal role in the regulation of systematic iron metabolism, erythropoiesis, and in the protection of liver from iron overload-evoked ferroptosis, fibrosis, and cirrhosis.1 Based on their novel findings, the authors propose a potential therapeutic strategy for mitigating a spectrum of iron overload disorders by targeting iron-evoked ferroptosis and/or the divalent metal transporter Slc39a14.