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Genetic Polymorphisms of Hypoxia-Inducible Factor-1 Alpha and Cardiovascular Disease in Hemodialysis Patients

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dc.contributor.authorZheng, Zhen Lon-
dc.contributor.authorHwang, Young-Hwan-
dc.contributor.authorKim, Seong Kyun-
dc.contributor.authorKim, Sejoong-
dc.contributor.authorRo, Han-
dc.contributor.authorLee, Hyun Hee-
dc.contributor.authorJoo, Kwon Wook-
dc.contributor.authorYang, Jaeseok-
dc.contributor.authorChung, Woo Kyung-
dc.contributor.authorSung, Su-Ah-
dc.contributor.authorSon, Min Jung-
dc.date.accessioned2012-05-24T01:38:12Z-
dc.date.available2012-05-24T01:38:12Z-
dc.date.issued2009-
dc.identifier.citationNEPHRON CLINICAL PRACTICE; Vol.113 2; C104-C111ko_KR
dc.identifier.issn1660-2110-
dc.identifier.urihttps://hdl.handle.net/10371/76380-
dc.description.abstractBackground: Hemodialysis patients are prone to ischemic events potentially aggravated by hypoxia. The key player in adaptation to hypoxia is hypoxia-inducible factor-1 alpha (HIF-1 alpha). Therefore, we investigated the association of HIF-1 alpha polymorphisms with ischemia/hypoxia-related events in hemodialysis patients. Methods: Patients on maintenance hemodialysis were enrolled from 4 training hospitals in Korea. Seven single nucleotide polymorphisms (SNP) of HIF-1 alpha were genotyped. The association of these SNP with hypoxia-related clinical outcomes (ischemic diseases and anemia) and cancer was analyzed. Results: A total of 376 patients participated in the study. No significant difference in genotype distribution was found between subjects with and without the hypoxia-related events. Three sets of linkage disequilibrium blocks were made for haplotype analyses (rs2783778 and rs7148720 in 5` upstream region; rs7143164 and rs10873142; rs2301113, rs11549465 and rs2057482). Of these, the CT haplotype in the first set was associated with both acute myocardial infarction and frequent intradialytic hypotension (acute myocardial infarction: adjusted odds ratio = 0.15, 95% CI: 0.03-0.69; frequent intradialytic hypotension: adjusted odds ratio = 0.29, 95% CI: 0.12-0.72). Conclusion: Genetic polymorphisms of HIF-1 alpha were associated with acute myocardial infarction and intradialytic hypotension in hemodialysis patients. Copyright (C) 2009 S. Karger AG, Baselko_KR
dc.language.isoenko_KR
dc.publisherKARGERko_KR
dc.subjectHemodialysisko_KR
dc.subjectHypoxia-inducible factor 1ko_KR
dc.subjectSingle nucleotide polymorphismko_KR
dc.titleGenetic Polymorphisms of Hypoxia-Inducible Factor-1 Alpha and Cardiovascular Disease in Hemodialysis Patientsko_KR
dc.typeArticleko_KR
dc.contributor.AlternativeAuthor황영환-
dc.contributor.AlternativeAuthor김성균-
dc.contributor.AlternativeAuthor김세중-
dc.contributor.AlternativeAuthor손민정-
dc.contributor.AlternativeAuthor노한-
dc.contributor.AlternativeAuthor성수아-
dc.contributor.AlternativeAuthor이현희-
dc.contributor.AlternativeAuthor정우경-
dc.contributor.AlternativeAuthor주권욱-
dc.contributor.AlternativeAuthor양재석-
dc.identifier.doi10.1159/000228542-
dc.citation.journaltitleNEPHRON CLINICAL PRACTICE-
dc.description.citedreferenceRius J, 2008, NATURE, V453, P807, DOI 10.1038/nature06905-
dc.description.citedreferencePercy MJ, 2008, NEW ENGL J MED, V358, P162-
dc.description.citedreferenceNangaku M, 2007, J MOL MED-JMM, V85, P1325, DOI 10.1007/s00109-007-0278-y-
dc.description.citedreferenceBelAiba RS, 2007, MOL BIOL CELL, V18, P4691, DOI 10.1091/mbc.E07-04-0391-
dc.description.citedreferenceHlatky MA, 2007, AM HEART J, V154, P1035, DOI 10.1016/j.ahj.2007.07.042-
dc.description.citedreferencePurcell S, 2007, AM J HUM GENET, V81, P559, DOI 10.1086/519795-
dc.description.citedreferenceHong JM, 2007, OSTEOARTHR CARTILAGE, V15, P688, DOI 10.1016/j.joca.2006.12.007-
dc.description.citedreferencePeng YJ, 2006, J PHYSIOL-LONDON, V577, P705, DOI 10.1113/jphysiol.2006.114033-
dc.description.citedreferenceKe QD, 2006, MOL PHARMACOL, V70, P1469, DOI 10.1124/mol.106.027029-
dc.description.citedreferenceImai E, 2006, KIDNEY INT, V69, P877, DOI 10.1038/sj.ki.5000088-
dc.description.citedreferenceKido M, 2005, J AM COLL CARDIOL, V46, P2116, DOI 10.1016/j.jacc.2005.08.045-
dc.description.citedreferenceYamada N, 2005, J CLIN ENDOCR METAB, V90, P5841, DOI 10.1210/jc.2005-0991-
dc.description.citedreferenceKim JH, 2005, ONCOL REP, V13, P859-
dc.description.citedreferenceOllerenshaw M, 2004, CANCER GENET CYTOGEN, V153, P122, DOI 10.1016/j.cancergencyto.2004.01.014-
dc.description.citedreferenceHerrero JA, 2002, RESP MED, V96, P487, DOI 10.1053/rmed.2002.1346-
dc.description.citedreferenceElson DA, 2001, GENE DEV, V15, P2520-
dc.description.citedreferenceVincent KA, 2000, CIRCULATION, V102, P2255-
dc.description.citedreferenceSUN MK, 1994, AM J PHYSIOL, V266, pR245-
dc.description.citedreferenceROMALDINI H, 1984, AM REV RESPIR DIS, V129, P780-
dc.description.tc1-
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College of Medicine/School of Medicine (의과대학/대학원)Internal Medicine (내과학전공)Journal Papers (저널논문_내과학전공)
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