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.

PINK1 deficiency in Parkinson's disease models causes toxic oxidized and iron-depleted CISD1 yet CISD1 removal benefits PINK1 mutant Drosophila indicating its potential as a therapeutic target for mitochondrial dysfunction and neurodegeneration.

Cancer metastasis modulator MEMO1 binds iron and is involved in regulating iron homeostasis in cancer cells.

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

Iron-chelating pyoverdines from environmental Pseudomonas spp. show promising antibacterial activity against key human pathogens through the induction of iron starvation, while associated toxicity for host systems remains low.

Iron content in neural stem cells controlled by glial ferritin is critical for self-renewal and proliferation of neural stem cells.

The most common Parkinson’s disease-associated mutation, LRRK2 G2019S, impairs mitophagy in clinically relevant cells within the mouse brain and this defect can be reversed using a novel LRRK2 inhibitor.

As worms age reduced glutathione together with increased ferrous iron increases frailty and leads to ferroptosis, which is amenable to therapeutic intervention.

The expansion of our understanding about the regulation of iron metabolism, erythropoiesis, and the crosstalk between them has enabled delineating the pathophysiology of multiple diseases and provided rationale for novel therapeutic interventions.