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Iron and the Reticuloendothelial System

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Iron Physiology and Pathophysiology in Humans

Part of the book series: Nutrition and Health ((NH))

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Abstract

Iron is an essential component for all cells and higher eukaryotes due to its central role for oxygen transport, electron transport during mitochondrial respiration, in forming a prosthetic group for central metabolic enzymes, and for the regulation of transcription via its role as the central component of ribonucleotide reductase 1–3]. Moreover, iron catalyzes the formation of hydroxyl radicals, which then modulate the binding affinity of critical transcription factors such as HIF-1 or NF-κB and thus affect the gene expression during inflammation [4]. Therefore, both iron overload and iron deficiency exert subtle effects on essential metabolic pathways and on the growth, proliferation, and differentiation of organisms. The tight control of iron homeostasis is thus a pre-requisite to maintain a sufficient supply of iron for essential metabolic pathways while avoiding the metals’ detrimental effects on tissue damage via radical formation. In addition, iron is centrally involved in the regulation of cellular immune function, while on the other hand, it is an essential nutrient for invading microbes and tumor cells. Specifically, microorganisms have evoked multiple strategies to capture and ingest iron, which they need for proliferation, pathogenicity, and defense pathways including biofilm formation [5]. The divergent pathways by which microorganisms can acquire iron have been recently reviewed [6, 7].

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Grant support by the Austrian Research Funds-FWF P-19664 is gratefully acknowledged.

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Weiss, G. (2012). Iron and the Reticuloendothelial System. In: Anderson, G., McLaren, G. (eds) Iron Physiology and Pathophysiology in Humans. Nutrition and Health. Humana Press. https://doi.org/10.1007/978-1-60327-485-2_11

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