Telomere length is shorter in healthy offspring of subjects with coronary artery disease: support for the telomere hypothesis
Background:Telomeres are shorter in subjects with coronary artery disease (CAD) and may indicate premature biological ageing. However, whether shorter telomeres are a primary abnormality or secondary to the disease is unclear.Objective:To investigate whether shorter telomeres are a primary abnormali...
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| Veröffentlicht in: | Heart (British Cardiac Society) 2008-04, Vol.94 (4), p.422-425 |
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| creator | Brouilette, S W Whittaker, A Stevens, S E van der Harst, P Goodall, A H Samani, N J |
| description | Background:Telomeres are shorter in subjects with coronary artery disease (CAD) and may indicate premature biological ageing. However, whether shorter telomeres are a primary abnormality or secondary to the disease is unclear.Objective:To investigate whether shorter telomeres are a primary abnormality or secondary to CAD, telomere lengths in healthy young adults with contrasting familial risk of CAD were compared.Design:Case–control study.Methods:Mean telomere restriction fragment (TRF) length in DNA from circulating leucocytes was determined by Southern blotting in 45 healthy offspring of subjects with premature CAD (case offspring) and 59 offspring from families without such a history (control offspring). Correlation in mean TRF length was also assessed in 67 offspring–parent pairs.Results:On average, a decrease of 27.5 (10.7) bp in mean TRF per year of age was found. The unadjusted mean TRF length was 6.34 kb (95% CI 6.13 to 6.55) for case offspring and 6.75 kb (95% CI 6.57 to 6.94) for offspring of controls (p = 0.004). The adjusted difference in mean TRF between case and control offspring was 472 bp (95% CI 253 to 691, p |
| doi_str_mv | 10.1136/hrt.2007.139675 |
| format | Article |
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However, whether shorter telomeres are a primary abnormality or secondary to the disease is unclear.Objective:To investigate whether shorter telomeres are a primary abnormality or secondary to CAD, telomere lengths in healthy young adults with contrasting familial risk of CAD were compared.Design:Case–control study.Methods:Mean telomere restriction fragment (TRF) length in DNA from circulating leucocytes was determined by Southern blotting in 45 healthy offspring of subjects with premature CAD (case offspring) and 59 offspring from families without such a history (control offspring). Correlation in mean TRF length was also assessed in 67 offspring–parent pairs.Results:On average, a decrease of 27.5 (10.7) bp in mean TRF per year of age was found. The unadjusted mean TRF length was 6.34 kb (95% CI 6.13 to 6.55) for case offspring and 6.75 kb (95% CI 6.57 to 6.94) for offspring of controls (p = 0.004). The adjusted difference in mean TRF between case and control offspring was 472 bp (95% CI 253 to 691, p<0.001), equivalent to about 17 years of age-related attrition in telomere length. Furthermore, there was a significant positive correlation in mean TRF length between offspring and their parents (r = 0.37, p = 0.002).Conclusion:These findings suggest that inheritance of shorter telomeres is associated with increased familial risk of CAD. They support the hypothesis that telomere length is a primary abnormality involved in the pathogenesis of CAD.</description><identifier>ISSN: 1355-6037</identifier><identifier>EISSN: 1468-201X</identifier><identifier>DOI: 10.1136/hrt.2007.139675</identifier><identifier>PMID: 18347373</identifier><language>eng</language><publisher>London: BMJ Publishing Group Ltd and British Cardiovascular Society</publisher><subject>Adult ; Age ; Atherosclerosis ; Biological and medical sciences ; Body mass index ; Cardiology. Vascular system ; Cardiovascular disease ; Case-Control Studies ; Cell cycle ; Chromosomes ; Coronary Artery Disease - genetics ; Coronary heart disease ; Coronary vessels ; Deoxyribonucleic acid ; DNA ; Family medical history ; Female ; Genetic Predisposition to Disease ; Genetic recombination ; Heart ; Humans ; Hypotheses ; Male ; Medical sciences ; Molecular weight ; Pathogenesis ; Polymorphism, Restriction Fragment Length ; Recruitment ; Senescence ; Telomerase ; Telomere - genetics ; Telomere - ultrastructure ; Yeast</subject><ispartof>Heart (British Cardiac Society), 2008-04, Vol.94 (4), p.422-425</ispartof><rights>2008 BMJ Publishing Group and British Cardiovascular Society</rights><rights>2008 INIST-CNRS</rights><rights>Copyright: 2008 2008 BMJ Publishing Group and British Cardiovascular Society</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b457t-60943414cc433532ecbd33bb9e744de90d1ff60b1179efc6dbf7338718deb693</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttp://heart.bmj.com/content/94/4/422.full.pdf$$EPDF$$P50$$Gbmj$$H</linktopdf><linktohtml>$$Uhttp://heart.bmj.com/content/94/4/422.full$$EHTML$$P50$$Gbmj$$H</linktohtml><link.rule.ids>114,115,314,776,780,3183,23550,27901,27902,77569,77600</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20171858$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18347373$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Brouilette, S W</creatorcontrib><creatorcontrib>Whittaker, A</creatorcontrib><creatorcontrib>Stevens, S E</creatorcontrib><creatorcontrib>van der Harst, P</creatorcontrib><creatorcontrib>Goodall, A H</creatorcontrib><creatorcontrib>Samani, N J</creatorcontrib><title>Telomere length is shorter in healthy offspring of subjects with coronary artery disease: support for the telomere hypothesis</title><title>Heart (British Cardiac Society)</title><addtitle>Heart</addtitle><description>Background:Telomeres are shorter in subjects with coronary artery disease (CAD) and may indicate premature biological ageing. However, whether shorter telomeres are a primary abnormality or secondary to the disease is unclear.Objective:To investigate whether shorter telomeres are a primary abnormality or secondary to CAD, telomere lengths in healthy young adults with contrasting familial risk of CAD were compared.Design:Case–control study.Methods:Mean telomere restriction fragment (TRF) length in DNA from circulating leucocytes was determined by Southern blotting in 45 healthy offspring of subjects with premature CAD (case offspring) and 59 offspring from families without such a history (control offspring). Correlation in mean TRF length was also assessed in 67 offspring–parent pairs.Results:On average, a decrease of 27.5 (10.7) bp in mean TRF per year of age was found. The unadjusted mean TRF length was 6.34 kb (95% CI 6.13 to 6.55) for case offspring and 6.75 kb (95% CI 6.57 to 6.94) for offspring of controls (p = 0.004). The adjusted difference in mean TRF between case and control offspring was 472 bp (95% CI 253 to 691, p<0.001), equivalent to about 17 years of age-related attrition in telomere length. Furthermore, there was a significant positive correlation in mean TRF length between offspring and their parents (r = 0.37, p = 0.002).Conclusion:These findings suggest that inheritance of shorter telomeres is associated with increased familial risk of CAD. They support the hypothesis that telomere length is a primary abnormality involved in the pathogenesis of CAD.</description><subject>Adult</subject><subject>Age</subject><subject>Atherosclerosis</subject><subject>Biological and medical sciences</subject><subject>Body mass index</subject><subject>Cardiology. Vascular system</subject><subject>Cardiovascular disease</subject><subject>Case-Control Studies</subject><subject>Cell cycle</subject><subject>Chromosomes</subject><subject>Coronary Artery Disease - genetics</subject><subject>Coronary heart disease</subject><subject>Coronary vessels</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>Family medical history</subject><subject>Female</subject><subject>Genetic Predisposition to Disease</subject><subject>Genetic recombination</subject><subject>Heart</subject><subject>Humans</subject><subject>Hypotheses</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Molecular weight</subject><subject>Pathogenesis</subject><subject>Polymorphism, Restriction Fragment Length</subject><subject>Recruitment</subject><subject>Senescence</subject><subject>Telomerase</subject><subject>Telomere - genetics</subject><subject>Telomere - ultrastructure</subject><subject>Yeast</subject><issn>1355-6037</issn><issn>1468-201X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkUtv1DAUhS0EomVgzQ5ZQnSBlKkdO3bSHYx4iQo2o6rqxrKdmyZDEgfbUZkF_x2PMhSJTb3xlf3dcx8HoZeUrCll4rz1cZ0TIteUVUIWj9Ap5aLMckKvH6eYFUUmCJMn6FkIO0IIr0rxFJ3QknHJJDtFv7fQuwE84B7G29jiLuDQOh_B427ELeg-tnvsmiZMvhtvU4TDbHZgY8B3XUqwzrtR-z3Wh6Q9rrsAOsBFwqYpCeHGeRxbwPFvpXY_ufQQuvAcPWl0H-DF8V6h7ccP283n7PL7py-bd5eZ4YWMaYSKM065tZyxguVgTc2YMRVIzmuoSE2bRhBDqaygsaI2jWSslLSswYiKrdDZIjt593OGENXQBQt9r0dwc1CScMI5ow-COSkpoXmZwNf_gTs3-zHNoKgsiahyls4KnS-U9S4ED41KOxzSrhQl6uCfSv6pg39q8S9lvDrqzmaA-h9_NCwBb46ADlb3jdej7cI9l4xPUxeHBrOF60KEX_f_2v9QIgkV6tvVRomb91c35TVRXxP_duHNsHuwyz_nasF-</recordid><startdate>20080401</startdate><enddate>20080401</enddate><creator>Brouilette, S W</creator><creator>Whittaker, A</creator><creator>Stevens, S E</creator><creator>van der Harst, P</creator><creator>Goodall, A H</creator><creator>Samani, N J</creator><general>BMJ Publishing Group Ltd and British Cardiovascular Society</general><general>BMJ</general><general>BMJ Publishing Group LTD</general><scope>BSCLL</scope><scope>IQODW</scope><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20080401</creationdate><title>Telomere length is shorter in healthy offspring of subjects with coronary artery disease: support for the telomere hypothesis</title><author>Brouilette, S W ; Whittaker, A ; Stevens, S E ; van der Harst, P ; Goodall, A H ; Samani, N J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b457t-60943414cc433532ecbd33bb9e744de90d1ff60b1179efc6dbf7338718deb693</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Adult</topic><topic>Age</topic><topic>Atherosclerosis</topic><topic>Biological and medical sciences</topic><topic>Body mass index</topic><topic>Cardiology. Vascular system</topic><topic>Cardiovascular disease</topic><topic>Case-Control Studies</topic><topic>Cell cycle</topic><topic>Chromosomes</topic><topic>Coronary Artery Disease - genetics</topic><topic>Coronary heart disease</topic><topic>Coronary vessels</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>Family medical history</topic><topic>Female</topic><topic>Genetic Predisposition to Disease</topic><topic>Genetic recombination</topic><topic>Heart</topic><topic>Humans</topic><topic>Hypotheses</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Molecular weight</topic><topic>Pathogenesis</topic><topic>Polymorphism, Restriction Fragment Length</topic><topic>Recruitment</topic><topic>Senescence</topic><topic>Telomerase</topic><topic>Telomere - genetics</topic><topic>Telomere - ultrastructure</topic><topic>Yeast</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Brouilette, S W</creatorcontrib><creatorcontrib>Whittaker, A</creatorcontrib><creatorcontrib>Stevens, S E</creatorcontrib><creatorcontrib>van der Harst, P</creatorcontrib><creatorcontrib>Goodall, A H</creatorcontrib><creatorcontrib>Samani, N J</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Heart (British Cardiac Society)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Brouilette, S W</au><au>Whittaker, A</au><au>Stevens, S E</au><au>van der Harst, P</au><au>Goodall, A H</au><au>Samani, N J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Telomere length is shorter in healthy offspring of subjects with coronary artery disease: support for the telomere hypothesis</atitle><jtitle>Heart (British Cardiac Society)</jtitle><addtitle>Heart</addtitle><date>2008-04-01</date><risdate>2008</risdate><volume>94</volume><issue>4</issue><spage>422</spage><epage>425</epage><pages>422-425</pages><issn>1355-6037</issn><eissn>1468-201X</eissn><abstract>Background:Telomeres are shorter in subjects with coronary artery disease (CAD) and may indicate premature biological ageing. However, whether shorter telomeres are a primary abnormality or secondary to the disease is unclear.Objective:To investigate whether shorter telomeres are a primary abnormality or secondary to CAD, telomere lengths in healthy young adults with contrasting familial risk of CAD were compared.Design:Case–control study.Methods:Mean telomere restriction fragment (TRF) length in DNA from circulating leucocytes was determined by Southern blotting in 45 healthy offspring of subjects with premature CAD (case offspring) and 59 offspring from families without such a history (control offspring). Correlation in mean TRF length was also assessed in 67 offspring–parent pairs.Results:On average, a decrease of 27.5 (10.7) bp in mean TRF per year of age was found. The unadjusted mean TRF length was 6.34 kb (95% CI 6.13 to 6.55) for case offspring and 6.75 kb (95% CI 6.57 to 6.94) for offspring of controls (p = 0.004). The adjusted difference in mean TRF between case and control offspring was 472 bp (95% CI 253 to 691, p<0.001), equivalent to about 17 years of age-related attrition in telomere length. Furthermore, there was a significant positive correlation in mean TRF length between offspring and their parents (r = 0.37, p = 0.002).Conclusion:These findings suggest that inheritance of shorter telomeres is associated with increased familial risk of CAD. They support the hypothesis that telomere length is a primary abnormality involved in the pathogenesis of CAD.</abstract><cop>London</cop><pub>BMJ Publishing Group Ltd and British Cardiovascular Society</pub><pmid>18347373</pmid><doi>10.1136/hrt.2007.139675</doi><tpages>4</tpages></addata></record> |
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| subjects | Adult Age Atherosclerosis Biological and medical sciences Body mass index Cardiology. Vascular system Cardiovascular disease Case-Control Studies Cell cycle Chromosomes Coronary Artery Disease - genetics Coronary heart disease Coronary vessels Deoxyribonucleic acid DNA Family medical history Female Genetic Predisposition to Disease Genetic recombination Heart Humans Hypotheses Male Medical sciences Molecular weight Pathogenesis Polymorphism, Restriction Fragment Length Recruitment Senescence Telomerase Telomere - genetics Telomere - ultrastructure Yeast |
| title | Telomere length is shorter in healthy offspring of subjects with coronary artery disease: support for the telomere hypothesis |
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