Structural and Genetic Bases of Arterial Stiffness
Abstract
Arterial stiffness has independent predictive value for cardiovascular events. We review data concerning the heritability of arterial stiffness, and propose an integrated view of the structural and genetic determinants of arterial stiffness, based on a candidate gene approach and recent studies on gene expression profile. Arterial stiffness seems to have a genetic component, which is largely independent of the influence of blood pressure and other cardiovascular risk factors. In animal models of essential hypertension (SHR and SHR-SP), structural modifications of the arterial wall include an increase in the number of elastin/smooth muscle cell (SMC) connections, and smaller fenestrations of the internal elastic lamina, possibly leading to redistribution of the mechanical load toward elastic materials. These modifications may give rise to mechanisms that explain why changes in arterial wall material accompanying wall hypertrophy in these animals are not associated with an increase in arterial stiffness. In monogenic connective tissue diseases (Marfan, Williams, and Ehlers-Danlos syndromes) and the corresponding animal models, precise characterization of the arterial phenotype makes it possible to determine the influence of abnormal genetically determined wall components on arterial stiffness. Such studies have highlighted the role of extracellular matrix signaling in the vascular wall and have shown that elastin and collagen not only display elasticity or rigidity but also are involved in the control of SMC function. These data provide strong evidence that arterial stiffness is affected by the amount and density of stiff wall material and the spatial organization of that material.
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Age-related arterial stiffening (arteriosclerosis) is associated with quantitatively less elastin and more collagen but is also associated with qualitative changes in the arterial wall.
“The well-known, age-related arterial stiffening process (arteriosclerosis) is associated with quantitatively less elastin and more collagen but is also associated with qualitative changes in the arterial wall.143,199,200”
From Vascular Contributions to Cognitive Impairment and Dementia: A Statement for Healthcare Professionals From the American Heart Association/American Stroke Association (2011) · cites this paper as [200]
The Essential Hypertension section (page unavailable) says central arteries stiffen with age, elastic fibers lose their orderly arrangement and undergo thinning and fragmentation, and collagenous material increases. These passages support age-related stiffening, increased collagen, and qualitative wall changes, but they do not establish a quantitative decrease in elastin content. (LLM, conf=0.84)
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- Authors
- Laurent, S., Boutouyrie, P., & Lacolley, P.
- Affiliations
- From the Department of Pharmacology and INSERM U652 (S.L, P.B.), Hôpital Européen Georges Pompidou, Paris; and INSERM U684 (P.L.), Vandoeuvre-les-Nancy, France.
- Inserm (FR)
- Venue
- Hypertension
- Published
- 2005-06
- Volume
- 45
- Issue
- 6
- Pages
- 1050-1055
- ISSN
- 0194-911X (ISSN-L)
- 1524-4563
- OpenAlex
- W2134756264
- Cited by
- 435
- References
- 55
- Citations by year
- 2026: 5 · 2025: 8 · 2024: 12 · 2023: 10 · 2022: 16 · 2021: 19 · 2020: 18 · 2019: 16 · 2018: 19 · 2017: 15 · 2016: 20 · 2015: 24 · 2014: 35 · 2013: 31 · 2012: 31
- FWCI
- 5.15
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Hypertension (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Disease Prevention
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Connective tissue disorders research
- Physical Sciences › Engineering › Biomedical Engineering › Elasticity and Material Modeling
- Keywords
- arterial stiffness, heritability, candidate genes, gene expression profiling, essential hypertension, spontaneously hypertensive rats, internal elastic lamina, elastin, smooth muscle cells, connective tissue diseases, Marfan syndrome, Williams syndrome, Ehlers-Danlos syndrome, extracellular matrix signaling, collagen, vascular biomechanics
- MeSH terms
- Animals, Arteries, Compliance, Humans, Hypertension, Vascular Diseases, Gene Expression, Gene Expression Profiling
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