Elastic fibres and vascular structure in hypertension

Arribas, Silvia M.; Hinek, Aleksander; González, M. C.

doi:10.1016/j.pharmthera.2005.12.003

Cited by 218 publications

(208 citation statements)

References 225 publications

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“…Age-related reductions in arterial compliance (known as arteriosclerosis) lead to increases in systolic blood pressure in the aorta, a major risk factor for the development of heart failure (Mitchell 2008;O'Rourke and Hashimoto 2007). It is still unclear, however, whether vascular hypertension is a cause, or symptom, of this arterial stiffening (Arribas et al 2006;McEniery et al 2007). In addition to heart failure, chronic hypertension is implicated as a major risk factor in the development of strokes (Nilsson 2005), renal failure (Lariviere and Lebel 2003) and aortic aneurysms (Lederle et al 2008).…”

Section: Vascularmentioning

confidence: 99%

Tissue elasticity and the ageing elastic fibre

Sherratt

2009

AGE

265

189

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The ability of elastic tissues to deform under physiological forces and to subsequently release stored energy to drive passive recoil is vital to the function of many dynamic tissues. Within vertebrates, elastic fibres allow arteries and lungs to expand and contract, thus controlling variations in blood pressure and returning the pulmonary system to a resting state. Elastic fibres are composite structures composed of a cross-linked elastin core and an outer layer of fibrillin microfibrils. These two components perform distinct roles; elastin stores energy and drives passive recoil, whilst fibrillin microfibrils direct elastogenesis, mediate cell signalling, maintain tissue homeostasis via TGFβ sequestration and potentially act to reinforce the elastic fibre. In many tissues reduced elasticity, as a result of compromised elastic fibre function, becomes increasingly prevalent with age and contributes significantly to the burden of human morbidity and mortality. This review considers how the unique molecular structure, tissue distribution and longevity of elastic fibres pre-disposes these abundant extracellular matrix structures to the accumulation of damage in ageing dermal, pulmonary and vascular tissues. As compromised elasticity is a common feature of ageing dynamic tissues, the development of strategies to prevent, limit or reverse this loss of function will play a key role in reducing age-related morbidity and mortality.

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Section: Vascularmentioning

confidence: 99%

Tissue elasticity and the ageing elastic fibre

Sherratt

2009

AGE

265

189

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“…These alterations include increases in the degradation and synthesis of collagen and the destruction and reconstruction of elastin fibers, which eventually lead to remodeling of the arterial wall and modifications of its mechanical properties.The mechanism by which hypertension accelerates atherogenesis remains unclear. Tensile stretch on vascular cells may influence cell behavior, such as proliferation, apoptosis, and alterations in gene expression of the ECM [17,29]. However, it is well established that the development of hypertension is associated with an increase in ECM proteins, including elastin, in the arterial wall.…”

Section: Discussionmentioning

confidence: 99%

“…Clinical data and characteristics of the study groups are given in table. This definition was given by the National High Pressure Education Program [17].…”

Section: Tissue Samplesmentioning

confidence: 99%

An increase of elastic tissue fibers in blood vessel walls of placental stem villi and differences in the thickness of blood vessel walls in third trimester pre-eclampsia pregnancies

et al. 2010

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AbstractThis study has goals of examining whether pre-eclampsia may lead to an increase of elastic tissue fibers in blood vessel walls of placental stem villi or whether there are differences in the thickness of blood vessel walls within these villi when compared to normotensive pregnant women. Non-infarcted placental tissue samples from 28 participants with uncomplicated pregnancies and 26 patients with pre-eclampsia were obtained. After routine histological procedures, the sections were processed either for conventional Verhoeff staining for the demonstration of elastic fiber system. Paraffine sections from placenta biopsies prepared for light microscopic examination were gathered. In uncomplicated pregnancies, terminal villi blood vessels were observed with no stained elastic tissue fibers in most areas. In the pre-eclampsia pregnancy of human placenta, the elastic fibers significiantly increased in terminal villi blood vessel walls which were dark in color, using Verhoeff’s tissue stain, when comparing with the uncomplicated pregnancy group. Our results indicate that an increase of elastic tissue fibers in blood vessels of placental stem villus and terminal villi, and also an increase of wall thickness during pre-eclampsia.

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“…The turnover rate for collagen and elastin is low in healthy arteries, but vascular pathology upsets the regulatory pathways that maintain this balance. In response to hypertension, the overexpression of both proinflammatory and proteinase-inhibitory molecules dramatically increases arterial ECM synthesis (Arribas et al, 2006;Jacob et al, 2001;Jacob, 2003). Elastin and elastic fibers are progressively degraded by enzymatic processes involving an age-related imbalance between anti-proteases and proteases.…”

Section: Introductionmentioning

confidence: 99%

“…Imbalance in matrix metalloproteinase/tissue inhibitors of metalloproteinases may contribute to alteration in collagen turnover and extracellular matrix remodelling. However, the ECM proteins synthesized in response to hypertension have a threedimensional architecture that is functionally less optimal than those deposited during fetal development and may play an important role in determining the modulus of pathological elastin tissue (Arribas et al, 2006;Jacob et al, 2001;Jacob, 2003). The increase of aortic stiffness is not only because of enzymatic degradation of elastin, but also is due to other mechanisms mainly including age-dependent increase in the collagen content and arterial wall thickening, non-enzymatic glycation of proteins (elastin and collagens), leading to the formation of deleterious advanced glycation end-products (AGEs) and related molecular cross-links which modify the tissue mechanical properties (Gibbons & Dzau, 1994;Corman et al, 1998;Lakatta, 2003;O'Routke, 2007).…”

Section: Introductionmentioning

confidence: 99%