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Interleukin-6 receptor pathways in coronary heart disease: a collaborative meta-analysis of 82 studies

Summary Background Persistent inflammation has been proposed to contribute to various stages in the pathogenesis of cardiovascular disease. Interleukin-6 receptor (IL6R) signalling propagates downstream inflammation cascades. To assess whether this pathway is causally relevant to coronary heart dise... Full description

Journal Title: LANCET 2012, Vol.379 (9822), p.1205-1213
Main Author: Sarwar, Nadeem
Other Authors: Butterworth, Adam S , Freitag, Daniel F , Gregson, John , Willeit, Peter , Gorman, Donal N , Gao, Pei , Saleheen, Danish , Rendon, Augusto , Nelson, Christopher P , Braund, Peter S , Hall, Alistair S , Chasman, Daniel I , Tybjærg-Hansen, Anne , Chambers, John C , Benjamin, Emelia J , Franks, Paul W , Clarke, Robert , Wilde, Arthur A. M , Trip, Mieke D , Steri, Maristella , Witteman, Jacqueline C. M , Qi, Lu , van der Schoot, C. Ellen , de Faire, Ulf , Erdmann, Jeanette , Stringham, Heather M , Koenig, Wolfgang , Rader, Daniel J , Melzer, David , Reich, David , Psaty, Bruce M , Kleber, Marcus E , Panagiotakos, Demosthenes B , Willeit, Johann , Wennberg, Patrik , Woodward, Mark , Adamovic, Svetlana , Rimm, Eric B , Meade, Tom W , Gillum, Richard F , Shaffer, Jonathan A , Hofman, Albert , Onat, Altan , Kastelein, John J. P
Format: Electronic Article Electronic Article
Language: English
Subjects:
Quelle: Alma/SFX Local Collection
Publisher: Kidlington: Elsevier Ltd
ID: ISSN: 0140-6736
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title: Interleukin-6 receptor pathways in coronary heart disease: a collaborative meta-analysis of 82 studies
format: Article
creator:
  • Sarwar, Nadeem
  • Butterworth, Adam S
  • Freitag, Daniel F
  • Gregson, John
  • Willeit, Peter
  • Gorman, Donal N
  • Gao, Pei
  • Saleheen, Danish
  • Rendon, Augusto
  • Nelson, Christopher P
  • Braund, Peter S
  • Hall, Alistair S
  • Chasman, Daniel I
  • Tybjærg-Hansen, Anne
  • Chambers, John C
  • Benjamin, Emelia J
  • Franks, Paul W
  • Clarke, Robert
  • Wilde, Arthur A. M
  • Trip, Mieke D
  • Steri, Maristella
  • Witteman, Jacqueline C. M
  • Qi, Lu
  • van der Schoot, C. Ellen
  • de Faire, Ulf
  • Erdmann, Jeanette
  • Stringham, Heather M
  • Koenig, Wolfgang
  • Rader, Daniel J
  • Melzer, David
  • Reich, David
  • Psaty, Bruce M
  • Kleber, Marcus E
  • Panagiotakos, Demosthenes B
  • Willeit, Johann
  • Wennberg, Patrik
  • Woodward, Mark
  • Adamovic, Svetlana
  • Rimm, Eric B
  • Meade, Tom W
  • Gillum, Richard F
  • Shaffer, Jonathan A
  • Hofman, Albert
  • Onat, Altan
  • Kastelein, John J. P
subjects:
  • Allmänmedicin
  • Articles
  • Biological and medical sciences
  • Cardiology. Vascular system
  • Cardiovascular disease
  • Cardiovascular diseases
  • Care and treatment
  • Causality
  • Cellular signal transduction
  • Clinical Medicine
  • Coronary Disease - genetics
  • Coronary Disease - immunology
  • Coronary heart disease
  • Cytokine receptors
  • Development and progression
  • Endocrinology and Diabetes
  • Endokrinologi och diabetes
  • Gene Frequency
  • General aspects
  • General Practice
  • Genetic aspects
  • Genetic variation
  • Genetic Variation - genetics
  • Heart
  • Humans
  • Inflammation Mediators - blood
  • Interleukin-6
  • Interleukins
  • Internal Medicine
  • Inventors
  • Klinisk medicin
  • Medical and Health Sciences
  • Medical research
  • Medical sciences
  • Medicin och hälsovetenskap
  • Orthopedics
  • Ortopedi
  • Physiological aspects
  • Receptors, Interleukin-6 - genetics
  • Risk Factors
  • Signal Transduction - genetics
  • Studies
  • Systematic review
  • Womens health
ispartof: LANCET, 2012, Vol.379 (9822), p.1205-1213
description: Summary Background Persistent inflammation has been proposed to contribute to various stages in the pathogenesis of cardiovascular disease. Interleukin-6 receptor (IL6R) signalling propagates downstream inflammation cascades. To assess whether this pathway is causally relevant to coronary heart disease, we studied a functional genetic variant known to affect IL6R signalling. Methods In a collaborative meta-analysis, we studied Asp358Ala (rs2228145) in IL6R in relation to a panel of conventional risk factors and inflammation biomarkers in 125 222 participants. We also compared the frequency of Asp358Ala in 51 441 patients with coronary heart disease and in 136 226 controls. To gain insight into possible mechanisms, we assessed Asp358Ala in relation to localised gene expression and to postlipopolysaccharide stimulation of interleukin 6. Findings The minor allele frequency of Asp358Ala was 39%. Asp358Ala was not associated with lipid concentrations, blood pressure, adiposity, dysglycaemia, or smoking (p value for association per minor allele ≥0·04 for each). By contrast, for every copy of 358Ala inherited, mean concentration of IL6R increased by 34·3% (95% CI 30·4–38·2) and of interleukin 6 by 14·6% (10·7–18·4), and mean concentration of C-reactive protein was reduced by 7·5% (5·9–9·1) and of fibrinogen by 1·0% (0·7–1·3). For every copy of 358Ala inherited, risk of coronary heart disease was reduced by 3·4% (1·8–5·0). Asp358Ala was not related to IL6R mRNA levels or interleukin-6 production in monocytes. Interpretation Large-scale human genetic and biomarker data are consistent with a causal association between IL6R-related pathways and coronary heart disease. Funding British Heart Foundation; UK Medical Research Council; UK National Institute of Health Research, Cambridge Biomedical Research Centre; BUPA Foundation.
language: eng
source: Alma/SFX Local Collection
identifier: ISSN: 0140-6736
fulltext: fulltext
issn:
  • 0140-6736
  • 1474-547X
  • 1474-547X
url: Link


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titleInterleukin-6 receptor pathways in coronary heart disease: a collaborative meta-analysis of 82 studies
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creatorSarwar, Nadeem ; Butterworth, Adam S ; Freitag, Daniel F ; Gregson, John ; Willeit, Peter ; Gorman, Donal N ; Gao, Pei ; Saleheen, Danish ; Rendon, Augusto ; Nelson, Christopher P ; Braund, Peter S ; Hall, Alistair S ; Chasman, Daniel I ; Tybjærg-Hansen, Anne ; Chambers, John C ; Benjamin, Emelia J ; Franks, Paul W ; Clarke, Robert ; Wilde, Arthur A. M ; Trip, Mieke D ; Steri, Maristella ; Witteman, Jacqueline C. M ; Qi, Lu ; van der Schoot, C. Ellen ; de Faire, Ulf ; Erdmann, Jeanette ; Stringham, Heather M ; Koenig, Wolfgang ; Rader, Daniel J ; Melzer, David ; Reich, David ; Psaty, Bruce M ; Kleber, Marcus E ; Panagiotakos, Demosthenes B ; Willeit, Johann ; Wennberg, Patrik ; Woodward, Mark ; Adamovic, Svetlana ; Rimm, Eric B ; Meade, Tom W ; Gillum, Richard F ; Shaffer, Jonathan A ; Hofman, Albert ; Onat, Altan ; Kastelein, John J. P
creatorcontribSarwar, Nadeem ; Butterworth, Adam S ; Freitag, Daniel F ; Gregson, John ; Willeit, Peter ; Gorman, Donal N ; Gao, Pei ; Saleheen, Danish ; Rendon, Augusto ; Nelson, Christopher P ; Braund, Peter S ; Hall, Alistair S ; Chasman, Daniel I ; Tybjærg-Hansen, Anne ; Chambers, John C ; Benjamin, Emelia J ; Franks, Paul W ; Clarke, Robert ; Wilde, Arthur A. M ; Trip, Mieke D ; Steri, Maristella ; Witteman, Jacqueline C. M ; Qi, Lu ; van der Schoot, C. Ellen ; de Faire, Ulf ; Erdmann, Jeanette ; Stringham, Heather M ; Koenig, Wolfgang ; Rader, Daniel J ; Melzer, David ; Reich, David ; Psaty, Bruce M ; Kleber, Marcus E ; Panagiotakos, Demosthenes B ; Willeit, Johann ; Wennberg, Patrik ; Woodward, Mark ; Adamovic, Svetlana ; Rimm, Eric B ; Meade, Tom W ; Gillum, Richard F ; Shaffer, Jonathan A ; Hofman, Albert ; Onat, Altan ; Kastelein, John J. P ; IL6R Genetics Consortium Emerging Risk Factors Collaboration ; Institutionen för medicin, avdelningen för samhällsmedicin och folkhälsa ; Wallenberg Laboratory ; Göteborgs universitet ; Gothenburg University ; Institute of Neuroscience and Physiology, Department of Physiology ; Institute of Medicine, School of Public Health and Community Medicine ; Sahlgrenska Academy ; Centre for Bone and Arthritis Research ; Sahlgrenska akademin ; Wallenberglaboratoriet ; Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi
descriptionSummary Background Persistent inflammation has been proposed to contribute to various stages in the pathogenesis of cardiovascular disease. Interleukin-6 receptor (IL6R) signalling propagates downstream inflammation cascades. To assess whether this pathway is causally relevant to coronary heart disease, we studied a functional genetic variant known to affect IL6R signalling. Methods In a collaborative meta-analysis, we studied Asp358Ala (rs2228145) in IL6R in relation to a panel of conventional risk factors and inflammation biomarkers in 125 222 participants. We also compared the frequency of Asp358Ala in 51 441 patients with coronary heart disease and in 136 226 controls. To gain insight into possible mechanisms, we assessed Asp358Ala in relation to localised gene expression and to postlipopolysaccharide stimulation of interleukin 6. Findings The minor allele frequency of Asp358Ala was 39%. Asp358Ala was not associated with lipid concentrations, blood pressure, adiposity, dysglycaemia, or smoking (p value for association per minor allele ≥0·04 for each). By contrast, for every copy of 358Ala inherited, mean concentration of IL6R increased by 34·3% (95% CI 30·4–38·2) and of interleukin 6 by 14·6% (10·7–18·4), and mean concentration of C-reactive protein was reduced by 7·5% (5·9–9·1) and of fibrinogen by 1·0% (0·7–1·3). For every copy of 358Ala inherited, risk of coronary heart disease was reduced by 3·4% (1·8–5·0). Asp358Ala was not related to IL6R mRNA levels or interleukin-6 production in monocytes. Interpretation Large-scale human genetic and biomarker data are consistent with a causal association between IL6R-related pathways and coronary heart disease. Funding British Heart Foundation; UK Medical Research Council; UK National Institute of Health Research, Cambridge Biomedical Research Centre; BUPA Foundation.
identifier
0ISSN: 0140-6736
1ISSN: 1474-547X
2EISSN: 1474-547X
3DOI: 10.1016/S0140-6736(11)61931-4
4PMID: 22421339
5CODEN: LANCAO
languageeng
publisherKidlington: Elsevier Ltd
subjectAllmänmedicin ; Articles ; Biological and medical sciences ; Cardiology. Vascular system ; Cardiovascular disease ; Cardiovascular diseases ; Care and treatment ; Causality ; Cellular signal transduction ; Clinical Medicine ; Coronary Disease - genetics ; Coronary Disease - immunology ; Coronary heart disease ; Cytokine receptors ; Development and progression ; Endocrinology and Diabetes ; Endokrinologi och diabetes ; Gene Frequency ; General aspects ; General Practice ; Genetic aspects ; Genetic variation ; Genetic Variation - genetics ; Heart ; Humans ; Inflammation Mediators - blood ; Interleukin-6 ; Interleukins ; Internal Medicine ; Inventors ; Klinisk medicin ; Medical and Health Sciences ; Medical research ; Medical sciences ; Medicin och hälsovetenskap ; Orthopedics ; Ortopedi ; Physiological aspects ; Receptors, Interleukin-6 - genetics ; Risk Factors ; Signal Transduction - genetics ; Studies ; Systematic review ; Womens health
ispartofLANCET, 2012, Vol.379 (9822), p.1205-1213
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0Sarwar, Nadeem
1Butterworth, Adam S
2Freitag, Daniel F
3Gregson, John
4Willeit, Peter
5Gorman, Donal N
6Gao, Pei
7Saleheen, Danish
8Rendon, Augusto
9Nelson, Christopher P
10Braund, Peter S
11Hall, Alistair S
12Chasman, Daniel I
13Tybjærg-Hansen, Anne
14Chambers, John C
15Benjamin, Emelia J
16Franks, Paul W
17Clarke, Robert
18Wilde, Arthur A. M
19Trip, Mieke D
20Steri, Maristella
21Witteman, Jacqueline C. M
22Qi, Lu
23van der Schoot, C. Ellen
24de Faire, Ulf
25Erdmann, Jeanette
26Stringham, Heather M
27Koenig, Wolfgang
28Rader, Daniel J
29Melzer, David
30Reich, David
31Psaty, Bruce M
32Kleber, Marcus E
33Panagiotakos, Demosthenes B
34Willeit, Johann
35Wennberg, Patrik
36Woodward, Mark
37Adamovic, Svetlana
38Rimm, Eric B
39Meade, Tom W
40Gillum, Richard F
41Shaffer, Jonathan A
42Hofman, Albert
43Onat, Altan
44Kastelein, John J. P
45IL6R Genetics Consortium Emerging Risk Factors Collaboration
46Institutionen för medicin, avdelningen för samhällsmedicin och folkhälsa
47Wallenberg Laboratory
48Göteborgs universitet
49Gothenburg University
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51Institute of Medicine, School of Public Health and Community Medicine
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53Centre for Bone and Arthritis Research
54Sahlgrenska akademin
55Wallenberglaboratoriet
56Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi
title
0Interleukin-6 receptor pathways in coronary heart disease: a collaborative meta-analysis of 82 studies
1LANCET
addtitleLancet
descriptionSummary Background Persistent inflammation has been proposed to contribute to various stages in the pathogenesis of cardiovascular disease. Interleukin-6 receptor (IL6R) signalling propagates downstream inflammation cascades. To assess whether this pathway is causally relevant to coronary heart disease, we studied a functional genetic variant known to affect IL6R signalling. Methods In a collaborative meta-analysis, we studied Asp358Ala (rs2228145) in IL6R in relation to a panel of conventional risk factors and inflammation biomarkers in 125 222 participants. We also compared the frequency of Asp358Ala in 51 441 patients with coronary heart disease and in 136 226 controls. To gain insight into possible mechanisms, we assessed Asp358Ala in relation to localised gene expression and to postlipopolysaccharide stimulation of interleukin 6. Findings The minor allele frequency of Asp358Ala was 39%. Asp358Ala was not associated with lipid concentrations, blood pressure, adiposity, dysglycaemia, or smoking (p value for association per minor allele ≥0·04 for each). By contrast, for every copy of 358Ala inherited, mean concentration of IL6R increased by 34·3% (95% CI 30·4–38·2) and of interleukin 6 by 14·6% (10·7–18·4), and mean concentration of C-reactive protein was reduced by 7·5% (5·9–9·1) and of fibrinogen by 1·0% (0·7–1·3). For every copy of 358Ala inherited, risk of coronary heart disease was reduced by 3·4% (1·8–5·0). Asp358Ala was not related to IL6R mRNA levels or interleukin-6 production in monocytes. Interpretation Large-scale human genetic and biomarker data are consistent with a causal association between IL6R-related pathways and coronary heart disease. Funding British Heart Foundation; UK Medical Research Council; UK National Institute of Health Research, Cambridge Biomedical Research Centre; BUPA Foundation.
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19General Practice
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39Risk Factors
40Signal Transduction - genetics
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creationdate2012
titleInterleukin-6 receptor pathways in coronary heart disease: a collaborative meta-analysis of 82 studies
authorSarwar, Nadeem ; Butterworth, Adam S ; Freitag, Daniel F ; Gregson, John ; Willeit, Peter ; Gorman, Donal N ; Gao, Pei ; Saleheen, Danish ; Rendon, Augusto ; Nelson, Christopher P ; Braund, Peter S ; Hall, Alistair S ; Chasman, Daniel I ; Tybjærg-Hansen, Anne ; Chambers, John C ; Benjamin, Emelia J ; Franks, Paul W ; Clarke, Robert ; Wilde, Arthur A. M ; Trip, Mieke D ; Steri, Maristella ; Witteman, Jacqueline C. M ; Qi, Lu ; van der Schoot, C. Ellen ; de Faire, Ulf ; Erdmann, Jeanette ; Stringham, Heather M ; Koenig, Wolfgang ; Rader, Daniel J ; Melzer, David ; Reich, David ; Psaty, Bruce M ; Kleber, Marcus E ; Panagiotakos, Demosthenes B ; Willeit, Johann ; Wennberg, Patrik ; Woodward, Mark ; Adamovic, Svetlana ; Rimm, Eric B ; Meade, Tom W ; Gillum, Richard F ; Shaffer, Jonathan A ; Hofman, Albert ; Onat, Altan ; Kastelein, John J. P
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languageeng
creationdate2012
topic
0Allmänmedicin
1Articles
2Biological and medical sciences
3Cardiology. Vascular system
4Cardiovascular disease
5Cardiovascular diseases
6Care and treatment
7Causality
8Cellular signal transduction
9Clinical Medicine
10Coronary Disease - genetics
11Coronary Disease - immunology
12Coronary heart disease
13Cytokine receptors
14Development and progression
15Endocrinology and Diabetes
16Endokrinologi och diabetes
17Gene Frequency
18General aspects
19General Practice
20Genetic aspects
21Genetic variation
22Genetic Variation - genetics
23Heart
24Humans
25Inflammation Mediators - blood
26Interleukin-6
27Interleukins
28Internal Medicine
29Inventors
30Klinisk medicin
31Medical and Health Sciences
32Medical research
33Medical sciences
34Medicin och hälsovetenskap
35Orthopedics
36Ortopedi
37Physiological aspects
38Receptors, Interleukin-6 - genetics
39Risk Factors
40Signal Transduction - genetics
41Studies
42Systematic review
43Womens health
toplevel
0peer_reviewed
1online_resources
creatorcontrib
0Sarwar, Nadeem
1Butterworth, Adam S
2Freitag, Daniel F
3Gregson, John
4Willeit, Peter
5Gorman, Donal N
6Gao, Pei
7Saleheen, Danish
8Rendon, Augusto
9Nelson, Christopher P
10Braund, Peter S
11Hall, Alistair S
12Chasman, Daniel I
13Tybjærg-Hansen, Anne
14Chambers, John C
15Benjamin, Emelia J
16Franks, Paul W
17Clarke, Robert
18Wilde, Arthur A. M
19Trip, Mieke D
20Steri, Maristella
21Witteman, Jacqueline C. M
22Qi, Lu
23van der Schoot, C. Ellen
24de Faire, Ulf
25Erdmann, Jeanette
26Stringham, Heather M
27Koenig, Wolfgang
28Rader, Daniel J
29Melzer, David
30Reich, David
31Psaty, Bruce M
32Kleber, Marcus E
33Panagiotakos, Demosthenes B
34Willeit, Johann
35Wennberg, Patrik
36Woodward, Mark
37Adamovic, Svetlana
38Rimm, Eric B
39Meade, Tom W
40Gillum, Richard F
41Shaffer, Jonathan A
42Hofman, Albert
43Onat, Altan
44Kastelein, John J. P
45IL6R Genetics Consortium Emerging Risk Factors Collaboration
46Institutionen för medicin, avdelningen för samhällsmedicin och folkhälsa
47Wallenberg Laboratory
48Göteborgs universitet
49Gothenburg University
50Institute of Neuroscience and Physiology, Department of Physiology
51Institute of Medicine, School of Public Health and Community Medicine
52Sahlgrenska Academy
53Centre for Bone and Arthritis Research
54Sahlgrenska akademin
55Wallenberglaboratoriet
56Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi
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1Elsevier:ScienceDirect:Open Access
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6Medline
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13Academic OneFile (A&I only)
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jtitleLANCET
delivery
delcategoryRemote Search Resource
fulltextfulltext
addata
au
0Sarwar, Nadeem
1Butterworth, Adam S
2Freitag, Daniel F
3Gregson, John
4Willeit, Peter
5Gorman, Donal N
6Gao, Pei
7Saleheen, Danish
8Rendon, Augusto
9Nelson, Christopher P
10Braund, Peter S
11Hall, Alistair S
12Chasman, Daniel I
13Tybjærg-Hansen, Anne
14Chambers, John C
15Benjamin, Emelia J
16Franks, Paul W
17Clarke, Robert
18Wilde, Arthur A. M
19Trip, Mieke D
20Steri, Maristella
21Witteman, Jacqueline C. M
22Qi, Lu
23van der Schoot, C. Ellen
24de Faire, Ulf
25Erdmann, Jeanette
26Stringham, Heather M
27Koenig, Wolfgang
28Rader, Daniel J
29Melzer, David
30Reich, David
31Psaty, Bruce M
32Kleber, Marcus E
33Panagiotakos, Demosthenes B
34Willeit, Johann
35Wennberg, Patrik
36Woodward, Mark
37Adamovic, Svetlana
38Rimm, Eric B
39Meade, Tom W
40Gillum, Richard F
41Shaffer, Jonathan A
42Hofman, Albert
43Onat, Altan
44Kastelein, John J. P
aucorp
0IL6R Genetics Consortium Emerging Risk Factors Collaboration
1Institutionen för medicin, avdelningen för samhällsmedicin och folkhälsa
2Wallenberg Laboratory
3Göteborgs universitet
4Gothenburg University
5Institute of Neuroscience and Physiology, Department of Physiology
6Institute of Medicine, School of Public Health and Community Medicine
7Sahlgrenska Academy
8Centre for Bone and Arthritis Research
9Sahlgrenska akademin
10Wallenberglaboratoriet
11Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi
formatjournal
genrearticle
ristypeJOUR
atitleInterleukin-6 receptor pathways in coronary heart disease: a collaborative meta-analysis of 82 studies
jtitleLANCET
addtitleLancet
date2012
risdate2012
volume379
issue9822
spage1205
epage1213
pages1205-1213
issn
00140-6736
11474-547X
eissn1474-547X
codenLANCAO
notesMembers listed at end of paper
abstractSummary Background Persistent inflammation has been proposed to contribute to various stages in the pathogenesis of cardiovascular disease. Interleukin-6 receptor (IL6R) signalling propagates downstream inflammation cascades. To assess whether this pathway is causally relevant to coronary heart disease, we studied a functional genetic variant known to affect IL6R signalling. Methods In a collaborative meta-analysis, we studied Asp358Ala (rs2228145) in IL6R in relation to a panel of conventional risk factors and inflammation biomarkers in 125 222 participants. We also compared the frequency of Asp358Ala in 51 441 patients with coronary heart disease and in 136 226 controls. To gain insight into possible mechanisms, we assessed Asp358Ala in relation to localised gene expression and to postlipopolysaccharide stimulation of interleukin 6. Findings The minor allele frequency of Asp358Ala was 39%. Asp358Ala was not associated with lipid concentrations, blood pressure, adiposity, dysglycaemia, or smoking (p value for association per minor allele ≥0·04 for each). By contrast, for every copy of 358Ala inherited, mean concentration of IL6R increased by 34·3% (95% CI 30·4–38·2) and of interleukin 6 by 14·6% (10·7–18·4), and mean concentration of C-reactive protein was reduced by 7·5% (5·9–9·1) and of fibrinogen by 1·0% (0·7–1·3). For every copy of 358Ala inherited, risk of coronary heart disease was reduced by 3·4% (1·8–5·0). Asp358Ala was not related to IL6R mRNA levels or interleukin-6 production in monocytes. Interpretation Large-scale human genetic and biomarker data are consistent with a causal association between IL6R-related pathways and coronary heart disease. Funding British Heart Foundation; UK Medical Research Council; UK National Institute of Health Research, Cambridge Biomedical Research Centre; BUPA Foundation.
copKidlington
pubElsevier Ltd
pmid22421339
doi10.1016/S0140-6736(11)61931-4
oafree_for_read