Dysregulated erythroblast-specific iron trafficking and regulation of iron metabolism provides evidence of a novel potential therapeutic target to reverse ineffective erythropoiesis in MDS.

In vivo studies reveal that mitochondrial Complex I deficiencies induce iron misregulation and liver iron overload that may contribute to neurodegeneration in mitochondrial disease mice, and that iron restriction is effective in reducing disease progression.

Iron derived from autophagy-mediated ferritin degradation in response to pressure overload induces lipid peroxidation, necrotic cardiomyocyte death, and heart failure in mice.

Under systemic iron overload, translational derepression of ferroportin mRNA via the IRE/IRP system antagonizes hepcidin-mediated ferroportin degradation to coordinately control serum iron.

The structural and mechanistic characterization of competitive inhibition of human DMT1 offers a promising route for the development of compounds for the treatment of iron overload disorders.

Post-menopausal women with atherosclerosis need to take the correct timing for hormone replacement therapy.

Heme accumulation is toxic, but deficiency of the heme transporter HRG1/SLC48A1 causes heme sequestration and crystallization into hemozoin within enlarged lysosomes of macrophages, thereby conferring heme tolerance to mammals.

The novel role of hepcidin in cell-autonomous iron regulation changes our understanding of tissue-specific iron control, and of its interplay with systemic iron homeostasis.

In Drosophila, the loss of Frataxin causes iron accumulation in the nervous system, which in turn enhances sphingolipid synthesis and activation of PDK1 and Mef2, which leads to neurodegeneration.

A decline in iron-recycling functions of the splenic red pulp macrophages early during aging is driven by iron loading and involves their damage and a loss in red blood cell clearance capacity.