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BioMed Research International
Volume 2013 (2013), Article ID 740573, 8 pages
http://dx.doi.org/10.1155/2013/740573
Review Article

Prooxidant Mechanisms in Iron Overload Cardiomyopathy

1Department of Medical Research, Tzu Chi General Hospital and Department of Pediatrics, Tzu Chi University, Hualien, Taiwan
2Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan

Received 5 June 2013; Accepted 28 October 2013

Academic Editor: Maha Zaki Rizk

Copyright © 2013 Ching-Feng Cheng and Wei-Shiung Lian. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Linked References

  1. M. G. Zurlo, D. P. Stefano, C. Borgna-Pignatti et al., “Survival and causes of death in thalassaemia major,” The Lancet, vol. 2, no. 8653, pp. 27–30, 1989. View at Scopus
  2. N. F. Olivieri and G. M. Brittenham, “Iron-chelating therapy and the treatment of thalassemia,” Blood, vol. 89, no. 3, pp. 739–761, 1997. View at Scopus
  3. E. D. Thomas, C. D. Buckner, and J. E. Sanders, “Marrow transplantation for thalassaemia,” The Lancet, vol. 2, no. 8292, pp. 227–229, 1982. View at Scopus
  4. I. Roberts, “Current status of allogeneic transplantation for haemoglobinopathies,” British Journal of Haematology, vol. 98, no. 1, pp. 1–7, 1997. View at Scopus
  5. “Third internationalsymposium on BMT in thalassemia,” Bone Marrow Transplant, vol. 19, supplement 2, pp. 1–206, 1997. View at Publisher · View at Google Scholar
  6. C. Giardini, M. Galimberti, G. Lucarelli et al., “Desferrioxamine therapy accelerates clearance of iron deposits after bone marrow transplantation for thalassaemia,” British Journal of Haematology, vol. 89, no. 4, pp. 868–873, 1995. View at Scopus
  7. P. Liu and N. Olivieri, “Iron overload cardiomyopathies: new insights into an old disease,” Cardiovascular Drugs and Therapy, vol. 8, no. 1, pp. 101–110, 1994. View at Publisher · View at Google Scholar · View at Scopus
  8. M. A. Aldouri, B. Wonke, A. V. Hoffbrand et al., “High incidence of cardiomyopathy in beta-thalassaemia patients receiving regular transfusion and iron chelation: reversal by intensified chelation,” Acta Haematologica, vol. 84, no. 3, pp. 113–117, 1990. View at Scopus
  9. J. W. Hou, M. H. Wu, K. H. Lin, and H.-C. Lue, “Prognostic significance of left ventricular diastolic indexes in β- thalassemia major,” Archives of Pediatrics and Adolescent Medicine, vol. 148, no. 8, pp. 862–866, 1994. View at Scopus
  10. M. A. Engle, M. Erlandson, and C. H. Smith, “Late cardiac complications of chronic, severe, refractory anemia with hemochromatosis,” Circulation, vol. 30, pp. 698–705, 1964. View at Scopus
  11. W. J. Bartfay, F. Dawood, W. H. Wen et al., “Cardiac function and cytotoxic aldehyde production in a murine model of chronic iron-overload,” Cardiovascular Research, vol. 43, no. 4, pp. 892–900, 1999. View at Publisher · View at Google Scholar · View at Scopus
  12. J. C. Wood, “Cardiac iron across different transfusion-dependent diseases,” Blood Reviews, vol. 22, supplement 2, pp. S14–S21, 2008. View at Publisher · View at Google Scholar · View at Scopus
  13. J. B. Porter, “Concepts and goals in the management of transfusional iron overload,” American Journal of Hematology, vol. 82, no. 12, pp. 1136–1139, 2007. View at Publisher · View at Google Scholar · View at Scopus
  14. G. Y. Oudit, M. G. Trivieri, N. Khaper, P. P. Liu, and P. H. Backx, “Role of L-type Ca2+ channels in iron transport and iron-overload cardiomyopathy,” Journal of Molecular Medicine, vol. 84, no. 5, pp. 349–364, 2006. View at Publisher · View at Google Scholar · View at Scopus
  15. C. Hershko, G. Link, and I. Cabantchik, “Pathophysiology of iron overload,” Annals of the New York Academy of Sciences, vol. 850, pp. 191–201, 1998. View at Publisher · View at Google Scholar · View at Scopus
  16. E. W. Randell, J. G. Parkes, N. F. Olivieri, and D. M. Templeton, “Uptake of non-transferrin-bound iron by both reductive and nonreductive processes is modulated by intracellular iron,” Journal of Biological Chemistry, vol. 269, no. 23, pp. 16046–16053, 1994. View at Scopus
  17. R. G. Tsushima, A. D. Wickenden, R. A. Bouchard, G. Y. Oudit, P. P. Liu, and P. H. Backx, “Modulation of iron uptake in heart by L-type Ca2+ channel modifiers: possible implications in iron overload,” Circulation Research, vol. 84, no. 11, pp. 1302–1309, 1999. View at Scopus
  18. G. Y. Oudit, H. Sun, M. G. Trivieri et al., “L-type Ca2+ channels provide a major pathway for iron entry into cardiomyocytes in iron-overload cardiomyopathy,” Nature Medicine, vol. 9, no. 9, pp. 1187–1194, 2003. View at Publisher · View at Google Scholar · View at Scopus
  19. D. T. Kremastinos, D. P. Tsiapras, G. A. Tsetsos, E. I. Rentoukas, H. P. Vretou, and P. K. Toutouzas, “Left ventricular diastolic Doppler characteristics in β-thalassemia major,” Circulation, vol. 88, no. 3, pp. 1127–1135, 1993. View at Scopus
  20. N. F. Olivieri, G. M. Brittenham, D. Matsui et al., “Iron-chelation therapy with oral deferipronein patients with thalassemia major,” New England Journal Medicine, vol. 332, no. 14, pp. 918–922, 1995. View at Publisher · View at Google Scholar
  21. S. Crowe and W. J. Bartfay, “Amlodipine decreases iron uptake and oxygen free radical production in the heart of chronically iron overloaded mice,” Biological Research for Nursing, vol. 3, no. 4, pp. 189–197, 2002. View at Scopus
  22. S. Kumfu, S. Chattipakorn, K. Chinda, S. Fucharoen, and N. Chattipakorn, “T-type calcium channel blockade improves survival and cardiovascular function in thalassemic mice,” European Journal of Haematology, vol. 88, no. 6, pp. 535–548, 2012. View at Publisher · View at Google Scholar · View at Scopus
  23. S. Kumfu, S. Chattipakorn, S. Fucharoen, and N. Chattipakorn, “Ferric iron uptake into cardiomyocytes of β-thalassemic mice is not through calcium channels,” Drug and Chemical Toxicology, vol. 36, no. 3, pp. 329–334, 2013. View at Publisher · View at Google Scholar
  24. A. O. Jorgensen, A. C.-Y. Shen, W. Arnold, P. S. McPherson, and K. P. Campbell, “The Ca2+-release channel/ryanodine receptor is localized in junctional and corbular sarcoplasmic reticulum in cardiac muscle,” Journal of Cell Biology, vol. 120, no. 4, pp. 969–980, 1993. View at Publisher · View at Google Scholar · View at Scopus
  25. E. Kim, S. N. Giri, and I. N. Pessah, “Iron(II) is a modulator of ryanodine-sensitive calcium channels of cardiac muscle sarcoplasmic reticulum,” Toxicology and Applied Pharmacology, vol. 130, no. 1, pp. 57–66, 1995. View at Publisher · View at Google Scholar · View at Scopus
  26. R. A. Rose, M. Sellan, J. A. Simpson et al., “Iron overload decreases CaV1.3-dependent L-type Ca2+ currents leading to bradycardia, altered electrical conduction, and atrial fibrillation,” Circulation, vol. 4, no. 5, pp. 733–742, 2011. View at Publisher · View at Google Scholar · View at Scopus
  27. G. J. Quinlan, T. W. Evans, and J. M. C. Gutteridge, “Iron and the redox status of the lungs,” Free Radical Biology and Medicine, vol. 33, no. 10, pp. 1306–1313, 2002. View at Publisher · View at Google Scholar · View at Scopus
  28. X. Gao, J. L. Campian, M. Qian, X. Sun, and J. W. Eaton, “Mitochondrial DNA damage in iron overload,” Journal of Biological Chemistry, vol. 284, no. 8, pp. 4767–4775, 2009. View at Publisher · View at Google Scholar · View at Scopus
  29. X. Gao, M. Qian, J. L. Campian et al., “Mitochondrial dysfunction may explain the cardiomyopathy of chronic iron overload,” Free Radical Biology and Medicine, vol. 49, no. 3, pp. 401–407, 2010. View at Publisher · View at Google Scholar · View at Scopus
  30. J. H. Jackson, I. U. Schraufstatter, P. A. Hyslop et al., “Role of oxidants in DNA damage. Hydroxyl radical mediates the synergistic DNA damaging effects of asbestos and cigarette smoke,” Journal of Clinical Investigation, vol. 80, no. 4, pp. 1090–1095, 1987. View at Scopus
  31. I. Schraufstatter, P. A. Hyslop, J. H. Jackson, and C. G. Cochrane, “Oxidant-induced DNA damage of target cells,” Journal of Clinical Investigation, vol. 82, no. 3, pp. 1040–1050, 1988. View at Scopus
  32. H. U. Enright, W. J. Miller, and R. P. Hebbel, “Nucleosomal histone protein protects DNA from iron-mediated damage,” Nucleic Acids Research, vol. 20, no. 13, pp. 3341–3346, 1992. View at Scopus
  33. H. Enright, K. A. Nath, R. P. Hebbel, and S. L. Schrier, “Internucleosomal cleavage of DNA is insufficient evidence to conclude that cell death is apoptotic,” Blood, vol. 83, no. 7, pp. 2005–2007, 1994. View at Scopus
  34. F. M. Yakes and B. Van Houten, “Mitochondrial DNA damage is more extensive and persists longer than nuclear DNA damage in human cells following oxidative stress,” Proceedings of the National Academy of Sciences of the United States of America, vol. 94, no. 2, pp. 514–519, 1997. View at Publisher · View at Google Scholar · View at Scopus
  35. J. J. Salazar and B. Van Houten, “Preferential mitochondrial DNA injury caused by glucose oxidase as a steady generator of hydrogen peroxide in human fibroblasts,” Mutation Research, vol. 385, no. 2, pp. 139–149, 1997. View at Publisher · View at Google Scholar · View at Scopus
  36. M. Shvartsman, R. Kikkeri, A. Shanzer, and Z. I. Cabantchik, “Non-transferrin-bound iron reaches mitochondria by a chelator-inaccessible mechanism: biological and clinical implications,” American Journal of Physiology, vol. 293, no. 4, pp. C1383–C1394, 2007. View at Publisher · View at Google Scholar · View at Scopus
  37. M. Shvartsman, E. Fibach, and Z. I. Cabantchik, “Transferrin-iron routing to the cytosol and mitochondria as studied by live and real-time fluorescence,” Biochemical Journal, vol. 429, no. 1, pp. 185–193, 2010. View at Publisher · View at Google Scholar · View at Scopus
  38. R. Bolli, B. S. Patel, W.-X. Zhu et al., “The iron chelator desferrioxamine attenuates postischemic ventricular dysfunction,” American Journal of Physiology, vol. 253, no. 6, pp. H1372–H1380, 1987. View at Scopus
  39. A. M. M. van der Kraaij, H. G. van Eijk, and J. F. Koster, “Prevention of postischemic cardiac injury by the orally active iron chelator 1,2-dimethyl-3-hydroxy-4-pyridone (L1) and the antioxidant (+)-cyanidanol-3,” Circulation, vol. 80, no. 1, pp. 158–164, 1989. View at Scopus
  40. W. S. Lian, H. Lin, W. T. K. Cheng, T. Kikuchi, and C. F. Cheng, “Granulocyte-CSF induced inflammation-associated cardiac thrombosis in iron loading mouse heart and can be attenuated by statin therapy,” Journal of Biomedical Science, vol. 18, p. 26, 2011. View at Publisher · View at Google Scholar · View at Scopus
  41. M. Harada, Y. Qin, H. Takano et al., “G-CSF prevents cardiac remodeling after myocardial infarction by activating the Jak-Stat pathway in cardiomyocytes,” Nature Medicine, vol. 11, no. 3, pp. 305–311, 2005. View at Publisher · View at Google Scholar · View at Scopus
  42. S. Minatoguchi, G. Takemura, X. Chen et al., “Acceleration of the healing process and myocardial regeneration may be important as a mechanism of improvement of cardiac function and remodeling by postinfarction granulocyte colony-stimulating factor treatment,” Circulation, vol. 109, no. 21, pp. 2572–2580, 2004. View at Publisher · View at Google Scholar · View at Scopus
  43. M. Ohtsuka, H. Takano, Y. Zou et al., “Cytokine therapy prevents left ventricular remodeling and dysfunction after myocardial infarction through neovascularization,” The FASEB Journal, vol. 18, no. 7, pp. 851–853, 2004. View at Scopus
  44. E. Deindl, M. Zaruba, S. Brunner et al., “G-CSF administration after myocardial infarction in mice attenuates late ischemic cardiomyopathy by enhanced arteriogenesis,” The FASEB Journal, vol. 20, no. 7, pp. 956–958, 2006. View at Publisher · View at Google Scholar · View at Scopus
  45. L. Li, G. Takemura, Y. Li et al., “Granulocyte colony-stimulating factor improves left ventricular function of doxorubicin-induced cardiomyopathy,” Laboratory Investigation, vol. 87, no. 5, pp. 440–455, 2007. View at Publisher · View at Google Scholar · View at Scopus
  46. S. M. Day, D. Duquaine, L. V. Mundada et al., “Chronic iron administration increases vascular oxidative stress and accelerates arterial thrombosis,” Circulation, vol. 107, no. 20, pp. 2601–2606, 2003. View at Scopus
  47. Z. Cheng, L. Ou, Y. Liu et al., “Granulocyte colony-stimulating factor exacerbates cardiac fibrosis after myocardial infarction in a rat model of permanent occlusion,” Cardiovascular Research, vol. 80, no. 3, pp. 425–434, 2008. View at Publisher · View at Google Scholar · View at Scopus
  48. Z. Cheng, X. Liu, L. Ou et al., “Mobilization of mesenchymal stem cells by granulocyte colony-stimulating factor in rats with acute myocardial infarction,” Cardiovascular Drugs and Therapy, vol. 22, no. 5, pp. 363–371, 2008. View at Publisher · View at Google Scholar · View at Scopus
  49. E. Stoyanova, G. Cloutier, H. Felfly, W. Lemsaddek, N. Ah-Son, and M. Trudel, “Evidence for a novel mechanism independent of myocardial iron in beta-thalassemia cardiac pathogenesis,” PloS ONE, vol. 7, Article ID e52128, 2012.
  50. L. C. Skow, B. A. Burkhart, and F. M. Johnson, “A mouse model for β-thalassemia,” Cell, vol. 34, no. 3, pp. 1043–1052, 1983. View at Scopus
  51. E. Stoyanova, M. Trudel, H. Felfly, D. Garcia, and G. Cloutier, “Characterization of circulatory disorders in β-thalassemic mice by noninvasive ultrasound biomicroscopy,” Physiological Genomics, vol. 29, no. 1, pp. 84–90, 2007. View at Publisher · View at Google Scholar · View at Scopus
  52. R. Mattera, G. P. Stone, N. Bahhur, and Y. A. Kuryshev, “Increased release of arachidonic acid and eicosanoids in iron-overloaded cardiomyocytes,” Circulation, vol. 103, no. 19, pp. 2395–2401, 2001. View at Scopus
  53. G. Johnson III, L. E. Furlan, N. Aoki, and A. M. Lefer, “Endothelium and myocardial protecting actions of taprostene, a stable prostacyclin analogue, after acute myocardial ischemia and reperfusion in cats,” Circulation Research, vol. 66, no. 5, pp. 1362–1370, 1990. View at Scopus
  54. H. Lin, H. F. Li, W. S. Lian et al., “Thromboxan A2 mediates iron-overload cardiomyopathy in mice through calcinurin-NFAT signaling pathway,” Circulation Journal, vol. 77, no. 10, pp. 2586–2595, 2013. View at Publisher · View at Google Scholar
  55. T. Cyrus, T. Ding, and D. Praticò, “Expression of thromboxane synthase, prostacyclin synthase and thromboxane receptor in atherosclerotic lesions: correlation with plaque composition,” Atherosclerosis, vol. 208, no. 2, pp. 376–381, 2010. View at Publisher · View at Google Scholar · View at Scopus
  56. N. G. Forouhi, A. H. Harding, M. Allison et al., “Elevated serum ferritin levels predict new-onset type 2 diabetes: results from the EPIC-Norfolk prospective study,” Diabetologia, vol. 50, no. 5, pp. 949–956, 2007. View at Publisher · View at Google Scholar · View at Scopus
  57. O. A. Mojiminiyi, R. Marouf, and N. A. Abdella, “Body iron stores in relation to the metabolic syndrome, glycemic control and complications in female patients with type 2 diabetes,” Nutrition, Metabolism and Cardiovascular Diseases, vol. 18, no. 8, pp. 559–566, 2008. View at Publisher · View at Google Scholar · View at Scopus
  58. B. J. Ku, S. Y. Kim, T. Y. Lee, and K. S. Park, “Serum ferritin is inversely correlated with serum adiponectin level: population-based cross-sectional study,” Disease Markers, vol. 27, no. 6, pp. 303–310, 2009. View at Publisher · View at Google Scholar · View at Scopus
  59. J. S. Gabrielsen, Y. Gao, J. A. Simcox et al., “Adipocyte iron regulates adiponectin and insulin sensitivity,” The Journal of Clinical Investigation, vol. 122, no. 10, pp. 3529–3540, 2012. View at Publisher · View at Google Scholar
  60. E. Kahn, M. Baarine, S. Pelloux et al., “Iron nanoparticles increase 7-ketocholesterol-induced cell death, inflammation, and oxidation on murine cardiac HL1-NB cells,” International Journal of Nanomedicine, vol. 5, no. 1, pp. 185–195, 2010. View at Scopus
  61. H. Lin, W. S. Lian, H. H. Chen, P. F. Lai, and C. F. Cheng, “Adiponectin ameliorates iron-overload cardiomyopathy through the PPARα-PGC-1-dependent signaling pathway,” Molecular Pharmacology, vol. 84, no. 2, pp. 275–285, 2013. View at Publisher · View at Google Scholar
  62. J. Davignon, “Beneficial cardiovascular pleiotropic effects of statins,” Circulation, vol. 109, no. 23, pp. III39–III43, 2004. View at Scopus
  63. J. K. Liao and U. Laufs, “Pleiotropic effects of statins,” Annual Review of Pharmacology and Toxicology, vol. 45, pp. 89–118, 2005. View at Publisher · View at Google Scholar · View at Scopus
  64. U. Grandel, L. Fink, A. Blum et al., “Endotoxin-induced myocardial tumor necrosis factor-α synthesis depresses contractility of isolated rat hearts: evidence for a role of sphingosine and cyclooxygenase-2-derived thromboxane production,” Circulation, vol. 102, no. 22, pp. 2758–2764, 2000. View at Scopus
  65. H. Katagiri, Y. Ito, S. Ito et al., “TNF-α induces thromboxane receptor signaling-dependent microcirculatory dysfunction in mouse liver,” Shock, vol. 30, no. 4, pp. 463–467, 2008. View at Publisher · View at Google Scholar · View at Scopus