Heritability and a Genome-Wide Linkage Scan for Arterial Stiffness, Wave Reflection, and Mean Arterial Pressure. The Framingham Heart Study

Gp, Mitchell; DeStefano, Anita L.; Larson, Martin G.

doi:10.1016/j.accreview.2005.10.027

Cited by 53 publications

(90 citation statements)

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“…3,4 Recently, the age and gender effects have been shown to be cross-cultural. 5 In addition to anthropometric factors, genetic epidemiology studies using family and twin data have provided verifiable evidence for a low to modest genetic contribution to PP with heritability estimates ranging from 0.13 using twins in the United Kingdom, 6 0.21 7 and 0.24 8 in European pedigrees, to 0.35 and 0.54 in American Caucasian 9 and African 10 families, respectively. An even higher heritability estimate of 0.63 was reported by a Swedish study.…”

Section: Introductionmentioning

confidence: 99%

“…12 The existence of a genetic contribution has warranted efforts to elucidate genes that affect PP, especially in recent years. For example, genetic marker-based linkage studies have identified multiple loci harboring susceptibility genes for PP in different populations, including Caucasians, 9,13,14 Mexicans, 15 American Indians 16 and African Americans. 17 The verification of susceptibility loci requires replication studies within and across populations to consolidate linkage results, which is especially important given the fact that inconsistent linkage results were reported by different studies.…”

Section: Introductionmentioning

confidence: 99%

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Genome-wide linkage and association scans for pulse pressure in Chinese twins

Zhang

Pang

et al. 2012

Hypertens Res

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Elevated pulse pressure (PP) is associated with cardiovascular disorders and mortality in various populations. The genetic influence on PP has been confirmed by heritability estimates using related individuals. Recently, efforts have been made by mapping genes that are linked to the phenotype. We report the results of our gene mapping studies conducted in the Chinese population in mainland China. The genome-wide linkage and association scans were carried out on 63 middle-aged dizygotic twin pairs using high-density markers. The linkage analysis identified three significant linkage peaks (all with a single point Po1e À05 ) on chromosome 11 (LOD core 4.06 at 30.5 cM), chromosome 12 (LOD score 3.97 at 100.7 cM) and chromosome 18 (LOD score 4.01 at 70.7 cM), with the last two peaks closely overlapping with linkage peaks reported by two American studies. Multiple regions with suggestive linkages were identified, with many of the peaks overlapping with published linkage regions. The genome-wide association analysis detected a suggestive association on chromosome 4 (rs17031508, Po8.34e À08 ) located within a wide region of suggestive linkage. Our results provide some evidence for genetic linkages and associations with PP in the Chinese population. Further investigation is warranted to replicate the findings and to explore the susceptibility loci or genes for PP.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Genome-wide linkage and association scans for pulse pressure in Chinese twins

Zhang

Pang

et al. 2012

Hypertens Res

View full text Add to dashboard Cite

show abstract

“…Besides anthropometric factors, genetic epidemiology studies using family and twin data have provided verifiable evidence for a low to modest genetic contribution in pulse pressure with heritability estimates ranging from 0.13 using twins in the UK (Snieder et al, 2000), 0.21 (Pilia et al, 2006) and 0.24 (van Rijn et al, 2007) in European pedigrees, to 0.35 and 0.54 in American Caucasian (Mitchell et al, 2005) and African families (Bochud et al, 2005). These results indicate that, similar to all other complex traits, the etiology of PP is complicated involving both genetic and environmental dissections (Turner & Boerwinkle, 2003).…”

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confidence: 99%

Heritability and Whole Genome Linkage of Pulse Pressure in Chinese Twin Pairs

et al. 2012

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Elevated pulse pressure is associated with cardiovascular disorders and mortality in various populations. The genetic influence on pulse pressure has been confirmed by heritability estimates using related individuals. Recently, efforts have been made in mapping genes that are linked to the phenotype. We report results on our heritability and linkage study conducted on the Chinese population in mainland China where cardiovascular and cerebrovascular diseases are becoming the leading cause of death. A total of 630 pairs of middle-aged Chinese twins were collected for heritability analysis, from which 63 dizygotic twin pairs were randomly selected for genome-wide linkage analysis using Affymetrix 6.0 SNP array. Regression analysis reconfirmed the significant effects of age, sex, and BMI on pulse pressure. Comparison of twin models suggested the parsimonious AE model as the best model with a heritability estimate of 0.45. Genome-wide non-parametric linkage analysis identified three significant linkage peaks on chromosome 11 (lod score 4.06 at 30.5 cM), chromosome 12 (lod score 3.97 at 100.7 cM), and chromosome 18 (lod score 4.01 at 70.7 cM) with the last two peaks closely overlapping with linkage peaks reported by two American studies. In addition, multiple regions with suggestive linkage were identified with many of them overlapping with published linkage regions. Our results provide both epidemiological and molecular genetic evidence for the genetic dissection of pulse pressure in the Chinese population, which could help in fine mapping and in characterizing genes that are involved in the regulation of pulse pressure.

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“…Also other indices of arterial stiffness, such as central augmentation index, carotid distensibility, pulse wave velocity, have a significant heritability, [8][9][10][11] and a locus on chromosome 2 has already been linked to pulse wave velocity. 9 Studies performed on animal models of essential hypertension and monogenic connective tissue diseases have highlighted the role of extracellular matrix signaling in the vascular wall beyond the effect of BP per se and in aortic wall tissues, the expression of 32 genes have been found to be associated with pulse wave velocity. 12 Thus, arterial stiffness seems to have a genetic component, which is largely independent of the influence of BP and other cardiovascular risk factors.…”

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confidence: 99%