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Review
. 2012;13(2):2368-86.
doi: 10.3390/ijms13022368. Epub 2012 Feb 22.

Impaired Iron Status in Aging Research

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Free PMC article
Review

Impaired Iron Status in Aging Research

Jinze Xu et al. Int J Mol Sci. .
Free PMC article

Abstract

Aging is associated with disturbances in iron metabolism and storage. During the last decade, remarkable progress has been made toward understanding their cellular and molecular mechanisms in aging and age-associated diseases using both cultured cells and animal models. The field has moved beyond descriptive studies to potential intervention studies focusing on iron chelation and removal. However, some findings remain controversial and inconsistent. This review summarizes important features of iron dyshomeostasis in aging research with a particular emphasis on current knowledge of the mechanisms underlying age-associated disorders in rodent models.

Keywords: aging; iron accumulation; labile iron; mitochondrial dysfunction; oxidative damage.

Figures

Figure 1
Figure 1
Cellular labile iron pool. The transferrin-transferrin receptor (Tf-TfR) pathway is the primary route of cellular iron acquisition [67]. Cells assimilate iron when Fe3+-Tf binds to TfR at the cell surface, and the complex is internalized into endosomes. Endosomal acidification promotes iron to dissociate from Tf, and the metal is then reduced to Fe2+ and transported into the cytosol by the transmembrane protein divalent metal transporter 1 (DMT1) and Zip14. The non-Tf-bound iron pathway, the shaded area, appears mainly during states of iron overload. Much of the iron normally assimilated by cells is destined to the mitochondria via mitoferrin, the site of heme and iron-sulfur cluster biosynthesis. Iron is exported from the mitochondria in the form of iron-sulfur clusters or heme. Export of iron-sulfur clusters involves ABCB7. Cells export iron through ferroportin. The absence of ferroportin in skeletal muscles and other post-mitotic tissues may result in iron accumulation over time.

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