Heme Oxygenase-1 Gene Promoter Microsatellite Polymorphism Is Associated With Progressive Atherosclerosis and Incident Cardiovascular Disease
OBJECTIVE—The enzyme heme oxygenase-1 (HO-1) exerts cytoprotective effects in response to various cellular stressors. A variable number tandem repeat polymorphism in the HO-1 gene promoter region has previously been linked to cardiovascular disease. We examined this association prospectively in the...
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| Veröffentlicht in: | Arteriosclerosis, thrombosis, and vascular biology thrombosis, and vascular biology, 2015-01, Vol.35 (1), p.229-236 |
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| creator | Pechlaner, Raimund Willeit, Peter Summerer, Monika Santer, Peter Egger, Georg Kronenberg, Florian Demetz, Egon Weiss, Günter Tsimikas, Sotirios Witztum, Joseph L Willeit, Karin Iglseder, Bernhard Paulweber, Bernhard Kedenko, Lyudmyla Haun, Margot Meisinger, Christa Gieger, Christian Müller-Nurasyid, Martina Peters, Annette Willeit, Johann Kiechl, Stefan |
| description | OBJECTIVE—The enzyme heme oxygenase-1 (HO-1) exerts cytoprotective effects in response to various cellular stressors. A variable number tandem repeat polymorphism in the HO-1 gene promoter region has previously been linked to cardiovascular disease. We examined this association prospectively in the general population.
APPROACH AND RESULTS—Incidence of stroke, myocardial infarction, or vascular death was registered between 1995 and 2010 in 812 participants of the Bruneck Study aged 45 to 84 years (49.4% males). Carotid atherosclerosis progression was quantified by high-resolution ultrasound. HO-1 variable number tandem repeat length was determined by polymerase chain reaction. Subjects with ≥32 tandem repeats on both HO-1 alleles compared with the rest of the population (recessive trait) featured substantially increased cardiovascular disease risk (hazard ratio [95% confidence interval], 5.45 [2.39, 12.42]; P |
| doi_str_mv | 10.1161/ATVBAHA.114.304729 |
| format | Article |
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APPROACH AND RESULTS—Incidence of stroke, myocardial infarction, or vascular death was registered between 1995 and 2010 in 812 participants of the Bruneck Study aged 45 to 84 years (49.4% males). Carotid atherosclerosis progression was quantified by high-resolution ultrasound. HO-1 variable number tandem repeat length was determined by polymerase chain reaction. Subjects with ≥32 tandem repeats on both HO-1 alleles compared with the rest of the population (recessive trait) featured substantially increased cardiovascular disease risk (hazard ratio [95% confidence interval], 5.45 [2.39, 12.42]; P<0.0001), enhanced atherosclerosis progression (median difference in atherosclerosis score [interquartile range], 2.1 [0.8, 5.6] versus 0.0 [0.0, 2.2] mm; P=0.0012), and a trend toward higher levels of oxidized phospholipids on apolipoprotein B-100 (median oxidized phospholipids/apolipoprotein B level [interquartile range], 11364 [4160, 18330] versus 4844 [3174, 12284] relative light units; P=0.0554). Increased cardiovascular disease risk in those homozygous for ≥32 repeats was also detected in a pooled analysis of 7848 participants of the Bruneck, SAPHIR, and KORA prospective studies (hazard ratio [95% confidence interval], 3.26 [1.50, 7.33]; P=0.0043).
CONCLUSIONS—This study found a strong association between the HO-1 variable number tandem repeat polymorphism and cardiovascular disease risk confined to subjects with a high number of repeats on both HO-1 alleles and provides evidence for accelerated atherogenesis and decreased antioxidant defense in this vascular high-risk group.</description><identifier>ISSN: 1079-5642</identifier><identifier>EISSN: 1524-4636</identifier><identifier>DOI: 10.1161/ATVBAHA.114.304729</identifier><identifier>PMID: 25359861</identifier><language>eng</language><publisher>United States: American Heart Association, Inc</publisher><subject>Aged ; Aged, 80 and over ; Apolipoprotein B-100 - blood ; Atherosclerosis - blood ; Atherosclerosis - diagnosis ; Atherosclerosis - enzymology ; Atherosclerosis - genetics ; Atherosclerosis - mortality ; Austria - epidemiology ; Cardiovascular Diseases - blood ; Cardiovascular Diseases - diagnosis ; Cardiovascular Diseases - enzymology ; Cardiovascular Diseases - genetics ; Cardiovascular Diseases - mortality ; Disease Progression ; Female ; Genetic Markers ; Genetic Predisposition to Disease ; Heme Oxygenase-1 - genetics ; Heterozygote ; Homozygote ; Humans ; Incidence ; Male ; Middle Aged ; Minisatellite Repeats ; Myocardial Infarction - enzymology ; Myocardial Infarction - genetics ; Myocardial Infarction - mortality ; Oxidation-Reduction ; Phenotype ; Phospholipids - blood ; Polymorphism, Genetic ; Promoter Regions, Genetic ; Proportional Hazards Models ; Prospective Studies ; Risk Factors ; Stroke - enzymology ; Stroke - genetics ; Stroke - mortality</subject><ispartof>Arteriosclerosis, thrombosis, and vascular biology, 2015-01, Vol.35 (1), p.229-236</ispartof><rights>2015 American Heart Association, Inc.</rights><rights>2014 American Heart Association, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4499-902767a95b3120148b87b7f745f19170f8d720aa337af99582e862f02a21791d3</citedby><cites>FETCH-LOGICAL-c4499-902767a95b3120148b87b7f745f19170f8d720aa337af99582e862f02a21791d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25359861$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pechlaner, Raimund</creatorcontrib><creatorcontrib>Willeit, Peter</creatorcontrib><creatorcontrib>Summerer, Monika</creatorcontrib><creatorcontrib>Santer, Peter</creatorcontrib><creatorcontrib>Egger, Georg</creatorcontrib><creatorcontrib>Kronenberg, Florian</creatorcontrib><creatorcontrib>Demetz, Egon</creatorcontrib><creatorcontrib>Weiss, Günter</creatorcontrib><creatorcontrib>Tsimikas, Sotirios</creatorcontrib><creatorcontrib>Witztum, Joseph L</creatorcontrib><creatorcontrib>Willeit, Karin</creatorcontrib><creatorcontrib>Iglseder, Bernhard</creatorcontrib><creatorcontrib>Paulweber, Bernhard</creatorcontrib><creatorcontrib>Kedenko, Lyudmyla</creatorcontrib><creatorcontrib>Haun, Margot</creatorcontrib><creatorcontrib>Meisinger, Christa</creatorcontrib><creatorcontrib>Gieger, Christian</creatorcontrib><creatorcontrib>Müller-Nurasyid, Martina</creatorcontrib><creatorcontrib>Peters, Annette</creatorcontrib><creatorcontrib>Willeit, Johann</creatorcontrib><creatorcontrib>Kiechl, Stefan</creatorcontrib><title>Heme Oxygenase-1 Gene Promoter Microsatellite Polymorphism Is Associated With Progressive Atherosclerosis and Incident Cardiovascular Disease</title><title>Arteriosclerosis, thrombosis, and vascular biology</title><addtitle>Arterioscler Thromb Vasc Biol</addtitle><description>OBJECTIVE—The enzyme heme oxygenase-1 (HO-1) exerts cytoprotective effects in response to various cellular stressors. A variable number tandem repeat polymorphism in the HO-1 gene promoter region has previously been linked to cardiovascular disease. We examined this association prospectively in the general population.
APPROACH AND RESULTS—Incidence of stroke, myocardial infarction, or vascular death was registered between 1995 and 2010 in 812 participants of the Bruneck Study aged 45 to 84 years (49.4% males). Carotid atherosclerosis progression was quantified by high-resolution ultrasound. HO-1 variable number tandem repeat length was determined by polymerase chain reaction. Subjects with ≥32 tandem repeats on both HO-1 alleles compared with the rest of the population (recessive trait) featured substantially increased cardiovascular disease risk (hazard ratio [95% confidence interval], 5.45 [2.39, 12.42]; P<0.0001), enhanced atherosclerosis progression (median difference in atherosclerosis score [interquartile range], 2.1 [0.8, 5.6] versus 0.0 [0.0, 2.2] mm; P=0.0012), and a trend toward higher levels of oxidized phospholipids on apolipoprotein B-100 (median oxidized phospholipids/apolipoprotein B level [interquartile range], 11364 [4160, 18330] versus 4844 [3174, 12284] relative light units; P=0.0554). Increased cardiovascular disease risk in those homozygous for ≥32 repeats was also detected in a pooled analysis of 7848 participants of the Bruneck, SAPHIR, and KORA prospective studies (hazard ratio [95% confidence interval], 3.26 [1.50, 7.33]; P=0.0043).
CONCLUSIONS—This study found a strong association between the HO-1 variable number tandem repeat polymorphism and cardiovascular disease risk confined to subjects with a high number of repeats on both HO-1 alleles and provides evidence for accelerated atherogenesis and decreased antioxidant defense in this vascular high-risk group.</description><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Apolipoprotein B-100 - blood</subject><subject>Atherosclerosis - blood</subject><subject>Atherosclerosis - diagnosis</subject><subject>Atherosclerosis - enzymology</subject><subject>Atherosclerosis - genetics</subject><subject>Atherosclerosis - mortality</subject><subject>Austria - epidemiology</subject><subject>Cardiovascular Diseases - blood</subject><subject>Cardiovascular Diseases - diagnosis</subject><subject>Cardiovascular Diseases - enzymology</subject><subject>Cardiovascular Diseases - genetics</subject><subject>Cardiovascular Diseases - mortality</subject><subject>Disease Progression</subject><subject>Female</subject><subject>Genetic Markers</subject><subject>Genetic Predisposition to Disease</subject><subject>Heme Oxygenase-1 - genetics</subject><subject>Heterozygote</subject><subject>Homozygote</subject><subject>Humans</subject><subject>Incidence</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Minisatellite Repeats</subject><subject>Myocardial Infarction - enzymology</subject><subject>Myocardial Infarction - genetics</subject><subject>Myocardial Infarction - mortality</subject><subject>Oxidation-Reduction</subject><subject>Phenotype</subject><subject>Phospholipids - blood</subject><subject>Polymorphism, Genetic</subject><subject>Promoter Regions, Genetic</subject><subject>Proportional Hazards Models</subject><subject>Prospective Studies</subject><subject>Risk Factors</subject><subject>Stroke - enzymology</subject><subject>Stroke - genetics</subject><subject>Stroke - mortality</subject><issn>1079-5642</issn><issn>1524-4636</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kcFOGzEQhq2KqlDgBXqo_AJLba_XXl-QltCSSFRwCHC0nN3ZrFvvOrI3oXmIvjOOElC59GJ7PPP9M5ofoS-UXFAq6Ldq_nhVTasU8IuccMnUB3RCC8YzLnJxlN5EqqwQnB2jzzH-IoRwxsgndMyKvFCloCfo7xR6wHd_tksYTISM4hsYAN8H3_sRAv5p6-CjGcE5O6Z_77a9D6vOxh7PIq5i9LVN6QY_2bHbccsAMdoN4GrsILG12502YjM0eDbUtoFhxBMTGus3JtZrZwK-thFS-zP0sTUuwvnhPkUPP77PJ9Ps9u5mNqlus5pzpTJFmBTSqGKRU0YoLxelXMhW8qKlikrSlo1kxJg8l6ZVqigZlIK1hBlGpaJNfoou97qr9aKHpk4TBeP0KtjehK32xur3mcF2euk3mudUMlEkAbYX2G0nBmjfWEr0zhx9MCcFXO_NSdDXf7u-Ia9upAKxL3j2Li0__nbrZwi6A-PG7n_KL5rfn5Q</recordid><startdate>201501</startdate><enddate>201501</enddate><creator>Pechlaner, Raimund</creator><creator>Willeit, Peter</creator><creator>Summerer, Monika</creator><creator>Santer, Peter</creator><creator>Egger, Georg</creator><creator>Kronenberg, Florian</creator><creator>Demetz, Egon</creator><creator>Weiss, Günter</creator><creator>Tsimikas, Sotirios</creator><creator>Witztum, Joseph L</creator><creator>Willeit, Karin</creator><creator>Iglseder, Bernhard</creator><creator>Paulweber, Bernhard</creator><creator>Kedenko, Lyudmyla</creator><creator>Haun, Margot</creator><creator>Meisinger, Christa</creator><creator>Gieger, Christian</creator><creator>Müller-Nurasyid, Martina</creator><creator>Peters, Annette</creator><creator>Willeit, Johann</creator><creator>Kiechl, Stefan</creator><general>American Heart Association, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>5PM</scope></search><sort><creationdate>201501</creationdate><title>Heme Oxygenase-1 Gene Promoter Microsatellite Polymorphism Is Associated With Progressive Atherosclerosis and Incident Cardiovascular Disease</title><author>Pechlaner, Raimund ; Willeit, Peter ; Summerer, Monika ; Santer, Peter ; Egger, Georg ; Kronenberg, Florian ; Demetz, Egon ; Weiss, Günter ; Tsimikas, Sotirios ; Witztum, Joseph L ; Willeit, Karin ; Iglseder, Bernhard ; Paulweber, Bernhard ; Kedenko, Lyudmyla ; Haun, Margot ; Meisinger, Christa ; Gieger, Christian ; Müller-Nurasyid, Martina ; Peters, Annette ; Willeit, Johann ; Kiechl, Stefan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4499-902767a95b3120148b87b7f745f19170f8d720aa337af99582e862f02a21791d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Apolipoprotein B-100 - blood</topic><topic>Atherosclerosis - blood</topic><topic>Atherosclerosis - diagnosis</topic><topic>Atherosclerosis - enzymology</topic><topic>Atherosclerosis - genetics</topic><topic>Atherosclerosis - mortality</topic><topic>Austria - epidemiology</topic><topic>Cardiovascular Diseases - blood</topic><topic>Cardiovascular Diseases - diagnosis</topic><topic>Cardiovascular Diseases - enzymology</topic><topic>Cardiovascular Diseases - genetics</topic><topic>Cardiovascular Diseases - mortality</topic><topic>Disease Progression</topic><topic>Female</topic><topic>Genetic Markers</topic><topic>Genetic Predisposition to Disease</topic><topic>Heme Oxygenase-1 - genetics</topic><topic>Heterozygote</topic><topic>Homozygote</topic><topic>Humans</topic><topic>Incidence</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Minisatellite Repeats</topic><topic>Myocardial Infarction - enzymology</topic><topic>Myocardial Infarction - genetics</topic><topic>Myocardial Infarction - mortality</topic><topic>Oxidation-Reduction</topic><topic>Phenotype</topic><topic>Phospholipids - blood</topic><topic>Polymorphism, Genetic</topic><topic>Promoter Regions, Genetic</topic><topic>Proportional Hazards Models</topic><topic>Prospective Studies</topic><topic>Risk Factors</topic><topic>Stroke - enzymology</topic><topic>Stroke - genetics</topic><topic>Stroke - mortality</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pechlaner, Raimund</creatorcontrib><creatorcontrib>Willeit, Peter</creatorcontrib><creatorcontrib>Summerer, Monika</creatorcontrib><creatorcontrib>Santer, Peter</creatorcontrib><creatorcontrib>Egger, Georg</creatorcontrib><creatorcontrib>Kronenberg, Florian</creatorcontrib><creatorcontrib>Demetz, Egon</creatorcontrib><creatorcontrib>Weiss, Günter</creatorcontrib><creatorcontrib>Tsimikas, Sotirios</creatorcontrib><creatorcontrib>Witztum, Joseph L</creatorcontrib><creatorcontrib>Willeit, Karin</creatorcontrib><creatorcontrib>Iglseder, Bernhard</creatorcontrib><creatorcontrib>Paulweber, Bernhard</creatorcontrib><creatorcontrib>Kedenko, Lyudmyla</creatorcontrib><creatorcontrib>Haun, Margot</creatorcontrib><creatorcontrib>Meisinger, Christa</creatorcontrib><creatorcontrib>Gieger, Christian</creatorcontrib><creatorcontrib>Müller-Nurasyid, Martina</creatorcontrib><creatorcontrib>Peters, Annette</creatorcontrib><creatorcontrib>Willeit, Johann</creatorcontrib><creatorcontrib>Kiechl, Stefan</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pechlaner, Raimund</au><au>Willeit, Peter</au><au>Summerer, Monika</au><au>Santer, Peter</au><au>Egger, Georg</au><au>Kronenberg, Florian</au><au>Demetz, Egon</au><au>Weiss, Günter</au><au>Tsimikas, Sotirios</au><au>Witztum, Joseph L</au><au>Willeit, Karin</au><au>Iglseder, Bernhard</au><au>Paulweber, Bernhard</au><au>Kedenko, Lyudmyla</au><au>Haun, Margot</au><au>Meisinger, Christa</au><au>Gieger, Christian</au><au>Müller-Nurasyid, Martina</au><au>Peters, Annette</au><au>Willeit, Johann</au><au>Kiechl, Stefan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Heme Oxygenase-1 Gene Promoter Microsatellite Polymorphism Is Associated With Progressive Atherosclerosis and Incident Cardiovascular Disease</atitle><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle><addtitle>Arterioscler Thromb Vasc Biol</addtitle><date>2015-01</date><risdate>2015</risdate><volume>35</volume><issue>1</issue><spage>229</spage><epage>236</epage><pages>229-236</pages><issn>1079-5642</issn><eissn>1524-4636</eissn><abstract>OBJECTIVE—The enzyme heme oxygenase-1 (HO-1) exerts cytoprotective effects in response to various cellular stressors. A variable number tandem repeat polymorphism in the HO-1 gene promoter region has previously been linked to cardiovascular disease. We examined this association prospectively in the general population.
APPROACH AND RESULTS—Incidence of stroke, myocardial infarction, or vascular death was registered between 1995 and 2010 in 812 participants of the Bruneck Study aged 45 to 84 years (49.4% males). Carotid atherosclerosis progression was quantified by high-resolution ultrasound. HO-1 variable number tandem repeat length was determined by polymerase chain reaction. Subjects with ≥32 tandem repeats on both HO-1 alleles compared with the rest of the population (recessive trait) featured substantially increased cardiovascular disease risk (hazard ratio [95% confidence interval], 5.45 [2.39, 12.42]; P<0.0001), enhanced atherosclerosis progression (median difference in atherosclerosis score [interquartile range], 2.1 [0.8, 5.6] versus 0.0 [0.0, 2.2] mm; P=0.0012), and a trend toward higher levels of oxidized phospholipids on apolipoprotein B-100 (median oxidized phospholipids/apolipoprotein B level [interquartile range], 11364 [4160, 18330] versus 4844 [3174, 12284] relative light units; P=0.0554). Increased cardiovascular disease risk in those homozygous for ≥32 repeats was also detected in a pooled analysis of 7848 participants of the Bruneck, SAPHIR, and KORA prospective studies (hazard ratio [95% confidence interval], 3.26 [1.50, 7.33]; P=0.0043).
CONCLUSIONS—This study found a strong association between the HO-1 variable number tandem repeat polymorphism and cardiovascular disease risk confined to subjects with a high number of repeats on both HO-1 alleles and provides evidence for accelerated atherogenesis and decreased antioxidant defense in this vascular high-risk group.</abstract><cop>United States</cop><pub>American Heart Association, Inc</pub><pmid>25359861</pmid><doi>10.1161/ATVBAHA.114.304729</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1079-5642 |
| ispartof | Arteriosclerosis, thrombosis, and vascular biology, 2015-01, Vol.35 (1), p.229-236 |
| issn | 1079-5642 1524-4636 |
| language | eng |
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| source | MEDLINE; Journals@Ovid Complete; Alma/SFX Local Collection |
| subjects | Aged Aged, 80 and over Apolipoprotein B-100 - blood Atherosclerosis - blood Atherosclerosis - diagnosis Atherosclerosis - enzymology Atherosclerosis - genetics Atherosclerosis - mortality Austria - epidemiology Cardiovascular Diseases - blood Cardiovascular Diseases - diagnosis Cardiovascular Diseases - enzymology Cardiovascular Diseases - genetics Cardiovascular Diseases - mortality Disease Progression Female Genetic Markers Genetic Predisposition to Disease Heme Oxygenase-1 - genetics Heterozygote Homozygote Humans Incidence Male Middle Aged Minisatellite Repeats Myocardial Infarction - enzymology Myocardial Infarction - genetics Myocardial Infarction - mortality Oxidation-Reduction Phenotype Phospholipids - blood Polymorphism, Genetic Promoter Regions, Genetic Proportional Hazards Models Prospective Studies Risk Factors Stroke - enzymology Stroke - genetics Stroke - mortality |
| title | Heme Oxygenase-1 Gene Promoter Microsatellite Polymorphism Is Associated With Progressive Atherosclerosis and Incident Cardiovascular Disease |
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