Hemochromatosis Protein (HFE) Knockout Mice As a Novel Model of Hemochromatosis: Implications for Study and Management of Iron-Overload Cardiomyopathy

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Hemochromatosis Protein (HFE) Knockout Mice As a Novel Model of Hemochromatosis: Implications for Study and Management of Iron-Overload Cardiomyopathy Pavel Zhabyeyev, PhD, Gavin Y. Oudit, MD, PhD, FRCPC Canadian Journal of Cardiology Volume 33, Issue 7, Pages 835-837 (July 2017) DOI: 10.1016/j.cjca.2017.04.013 Copyright © 2017 Canadian Cardiovascular Society Terms and Conditions

Figure 1 Iron homeostasis, primary hemochromatosis, and iron-overload cardiomyopathy. (A) Molecular mechanism of iron homeostasis. (B) Accumulation of non–transferrin-bound (NTBI) iron (Fe) in hereditary hemochromatosis. (C) Development of diastolic dysfunction and iron-overload cardiomyopathy caused by excess NTBI. BMP, bone morphogenetic protein; BMPR, BMP receptor; HFE, human hemochromatosis protein; HJV, hemojuvelin; mtDNA, mitochondrial DNA; TfR1 and TfR2, transferrin receptors 1 and 2, respectively. Canadian Journal of Cardiology 2017 33, 835-837DOI: (10.1016/j.cjca.2017.04.013) Copyright © 2017 Canadian Cardiovascular Society Terms and Conditions