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Iron, oxidative stress, and redox signaling in the cardiovascular system
Author(s) -
Gudjoncik Aurélie,
Guenancia Charles,
Zeller Marianne,
Cottin Yves,
Vergely Catherine,
Rochette Luc
Publication year - 2014
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201400036
Subject(s) - oxidative stress , ferroportin , hepcidin , microbiology and biotechnology , intracellular , chemistry , redox , oxidative phosphorylation , extracellular , regulator , biochemistry , dmt1 , homeostasis , iron deficiency , hemoglobin , heme , biology , metabolism , inflammation , medicine , anemia , transporter , immunology , iron homeostasis , organic chemistry , gene , enzyme
The redox state of the cell is predominantly dependent on an iron redox couple and is maintained within strict physiological limits. Iron is an essential metal for hemoglobin synthesis in erythrocytes, for oxidation–reduction reactions, and for cellular proliferation. The maintenance of stable iron concentrations requires the coordinated regulation of iron transport into plasma from dietary sources in the duodenum, from recycled senescent red cells in macrophages, and from storage in hepatocytes. The absorption of dietary iron, which is present in heme or nonheme form, is carried out by mature villus enterocytes of the duodenum and proximal jejunum. Multiple physiological processes are involved in maintaining iron homeostasis. These include its storage at the intracellular and extracellular level. Control of iron balance in the whole organism requires communication between sites of uptake, utilization, and storage. Key protein transporters and the molecules that regulate their activities have been identified. In this field, ferritins and hepcidin are the major regulator proteins. A variety of transcription factors may be activated depending on the level of oxidative stress, leading to the expression of different genes. Major preclinical and clinical trials have shown advances in iron‐chelation therapy for the treatment of iron‐overload disease as well as cardiovascular and chronic inflammatory diseases.