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Molecular pathogenesis of hereditary hemochromatosis

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dc.contributor.authorLiu, Jingqi
dc.contributor.authorPu, Chunwen
dc.contributor.authorLang, Lang
dc.contributor.authorQiao, Liang
dc.contributor.authorAbdullahi, Mohamud Abukar Haji
dc.contributor.authorJiang, Chunmeng
dc.date.accessioned2021-10-20T11:52:49Z
dc.date.available2021-10-20T11:52:49Z
dc.date.issued2016
dc.description.abstract. Hereditary hemochromatosis (HH) is an inherited iron overload disorder characterized by normal iron-driven erythropoiesis and abnormal iron metabolism, leading to excess iron deposited in parenchymal cells of liver, heart, and endocrine glands. Iron hormone, hepcidin, plays a critical role in iron homeostasis through interaction with ferroportin (FPN), a major cellular iron exporter. Hepcidin is encoded by hepcidin antimicrobial peptide (HAMP). Mutations in hepcidin and any genes that regulate the biology of hepcidin, including hemochromatosis genes (HFE), Hemojuvelin (HJV), transferring receptor 2 (TFR2) and FPN, result in hemochromatosis. The identification of hepcidin and its role will provide a better understanding for pathogenesis of HH.es
dc.formatapplication/pdfes
dc.format.extent8es
dc.identifier.citationHistology and Histopathology, Vol.31, nÂş8, (2016)
dc.identifier.doiDOI: 10.14670/HH-11-762
dc.identifier.issn0213-3911
dc.identifier.issn1699-5848
dc.identifier.urihttp://hdl.handle.net/10201/113085
dc.languageenges
dc.publisherUniversidad de Murcia. Departamento de BiologĂ­a Celular e HistologĂ­aes
dc.relationSin financiaciĂłn externa a la Universidades
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectHemochromatosises
dc.subjectHepcidines
dc.subjectHFEes
dc.subjectHJV FPNes
dc.subject.otherCDU::6 - Ciencias aplicadas::61 - Medicina::616 - PatologĂ­a. Medicina clĂ­nica. OncologĂ­aes
dc.titleMolecular pathogenesis of hereditary hemochromatosises
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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Histology and histopathology Vol.31, nÂş8 (2016)