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The underlying mechanism involves the upregulation of FOXN1 and FOXN1-regulated chemokines

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Abbreviations MDS Myelodysplastic syndromes SCD Sickle cell disease IOC Iron overload cardiomyopathy NTBI Non-transferrin-bound iron LPI Labile plasma iron DMT1 Divalent metal transporter 1 ZIP14 ZRT/IRT-like protein 14 LCN-2 Lipocalin-2 TTCC T-type calcium channels LTCC L-type calcium channels LCI Labile cellular iron LIP Labile iron pool FeS clusters Iron-sulfur clusters DFP Deferiprone ETC Electron transport chain IMM Inner mitochondrial membrane OXPHOS Oxidative phosphorylation ROS Reactive oxygen species Mfrn Mitoferrin MCU Mitochondrial calcium uniporter RIRR ROS-induced ROS release mPTP Mitochondrial permeability transition pore m Mitochondrial membrane potential mtDNA Mitochondrial DNA BCL-2 B-cell lymphoma-2 SS Szeto-Schiller PCD Programmed cell death BMMSCs Bone marrow mesenchymal stromal cells MAPK Mitogen-activated protein kinase MOMP Mitochondrial outer membrane permeabilization DAMPs Damage-associated molecular patterns OPA1 Optic atrophy 1 Drp1 Dynamin related protein 1 Fis1 Fission 1 RET Reverse electron transport CoQ Coenzyme Q10 TPP+ Triphenylphosphonium PGC-1 Peroxisome proliferator-activated receptor-gamma coactivator-1alpha KD Ketogenic diet PPAR Peroxisome proliferators-activated receptor SIRT Sirutin Author contributions Yangyang Zhao wrote the manuscript

A consequence of the existed TrxR1 complex in serum seems to be protection of the non-reduced TrxR1 from responding to certain electrophilic reagents