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Copyright: ©Author(s) 2026.
World J Diabetes. Jul 15, 2026; 17(7): 120448
Published online Jul 15, 2026. doi: 10.4239/wjd.120448
Figure 2
Figure 2 Iron homeostasis and mitochondrial iron metabolism in cardiomyocytes Schematic representation of iron uptake, intracellular transport, storage, and mitochondrial utilization in cardiomyocytes. Upon entering the mitochondrial matrix, iron can be channeled to three pathways: Heme biosynthesis, iron-sulfur (Fe-S) cluster biogenesis, or storage in mitochondrial ferritin (FtMt). Cytosolic Fe²+ comprises the labile iron pool, which is either stored in ferritin or exported via ferroportin, whose activity is negatively regulated by hepcidin. Upon entering the mitochondrial matrix, iron can be channeled to three pathways: Heme biosynthesis, iron-sulfur (Fe-S) cluster biogenesis, or storage in FtMt. ABCB7 and ABCB8 mediate Fe-S cluster export and mitochondrial iron efflux, respectively. Created with BioRender. Fe-S: Iron-sulfur; FtMt: Mitochondrial ferritin; LIP: Labile iron pool.


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