Cyclic Stretching Stimulates Synthesis of Matrix Components by Arterial Smooth Muscle Cells in Vitro

Leung, Donald Y.M.; Glagov, Seymour; Mathews, Martin B.

doi:10.1126/science.128820

Cited by 626 publications

(191 citation statements)

References 13 publications

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“…Agerelated arterial remodeling is primarily an adaptive response of the arterial wall to progressive elevations in chronic arterial BP 30) . The results of animal and human studies indicated that an increase in distending pressure is a major stimulus for hypertrophy of smooth muscle cells and the synthesis of extracellular matrix in the arterial wall [31][32][33][34] . Repeated intense cyclic stress may cause fracture of the load-bearing elastin fibers and thus dilation of the lumen 11) .…”

Section: Discussionmentioning

confidence: 99%

Attenuated Age-Related Carotid Arterial Remodeling in Adults with a High Level of Cardiorespiratory Fitness

Gando

Yamamoto

Kawano

et al. 2011

JAT

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Aim: Cardiorespiratory fitness (CRF) is independently associated with a reduced risk of cardiovascular disease. Carotid arterial remodeling, which is derived from the interplay between carotid luminal dilation and wall thickening, is also an independent predictor of cardiovascular events. We hypothesized that high CRF may be associated with reduced age-related carotid arterial remodeling. This cross-sectional study was performed to determine the relationships between CRF and age-related luminal dilation and wall thickening.

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Section: Discussionmentioning

confidence: 99%

Attenuated Age-Related Carotid Arterial Remodeling in Adults with a High Level of Cardiorespiratory Fitness

Gando

Yamamoto

Kawano

et al. 2011

JAT

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“…That the blebs were characterized by a decreased procollagen expression and decreased elastin content as compared with the adjacent AAA wall 68 again gives rise to the possibility that increased mechanical forces alter local ECM synthesis. This possibility is strengthened by findings that mechanical forces alter ECM production by smooth muscle cells (SMCs), 69 endothelial cells, 70 and other cells 71 in culture. Mechanical forces may also act to alter ECM synthesis in an indirect manner by stimulating cellular release of cytokines such as tumor necrosis factor-␣, 72 which inhibits procollagen expression in human aortic SMCs.…”

Section: Stress-mediated or Strain-mediated Wall Weakeningmentioning

confidence: 98%

Biomechanical Determinants of Abdominal Aortic Aneurysm Rupture

Vorp

Geest

2005

ATVB

231

172

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Abstract-Rupture of abdominal aortic aneurysm (AAA) represents a significant clinical event, having a mortality rate of 90% and being currently ranked as the 13th leading cause of death in the US. The ability to reliably evaluate the susceptibility of a particular AAA to rupture on a case-specific basis could vastly improve the clinical management of these patients. Because AAA rupture represents a mechanical failure of the degenerated aortic wall, biomechanical considerations are important to understand this process and to improve our predictions of its occurrence. Presented here is an overview of research to date related to the biomechanics of AAA rupture. This includes a summary of results related to ex vivo and in vivo mechanical testing, noninvasive AAA wall stress estimations, and potential mechanisms of AAA wall weakening. We conclude with a demonstration of a biomechanics-based approach to predicting AAA rupture on a patient-specific basis, which may ultimately prove to be superior to the widely and currently used maximum diameter criterion. Key Words: abdominal aortic aneurysm Ⅲ biomechanics Ⅲ rupture Ⅲ strength Ⅲ stress A bdominal aortic aneurysm (AAA) is a focal enlargement of the infrarenal aorta, which occurs over a time course of several years. This condition is present in Ϸ2% of the elderly population, with Ϸ150 000 new cases diagnosed each year, and the incidence is increasing. 1,2 If left untreated, AAA will gradually expand until rupture; it is an event that carries a mortality rate of 90% and that is ranked as the 13th most common cause of death in the US. 3 Current AAA repair procedures are expensive and carry significant morbidity and mortality risks.Open repair of AAA is a major surgical procedure that requires patients to be hospitalized typically for 1 week and to recuperate at home for several more weeks. The mean postoperative mortality for elective repair is Ϸ5% and for emergency operations 47% (range 27% to 69%). 4 The major drawback of open repair is the compromised quality of life after surgery because of postoperative pain, the prolonged recovery period, and the high costs associated with both the surgery and the recovery.An alternative approach that avoids the extensive tissue dissection associated with open repair is the minimally invasive endovascular repair procedure. The potential advantages of endovascular AAA repair include reductions in mortality, morbidity, blood loss, hospital stay, intensive careOriginal

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“…Both mechanical stimuli and biochemical signals regulate the interaction between the ECM and vascular cells Mack 2011;Humphrey et al 2015). Changes in the ECM are sensed by vascular cells through matrix-binding receptors, such as integrins, and influence cell migration, proliferation, and survival (Moiseeva 2001); in turn, vascular cells can modify the composition and structure of the ECM by increasing or decreasing secretion of matrix proteins and matrix-remodeling enzymes (Leung et al 1976;O'Callaghan and Williams 2000).…”

Section: Structure Of the Arterial Vessel Wallmentioning

confidence: 99%

TGF-β Family Signaling in Connective Tissue and Skeletal Diseases

MacFarlane

Haupt

Dietz

et al. 2017

Cold Spring Harb Perspect Biol

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The transforming growth factor b (TGF-b) family of signaling molecules, which includes TGF-bs, activins, inhibins, and numerous bone morphogenetic proteins (BMPs) and growth and differentiation factors (GDFs), has important functions in all cells and tissues, including soft connective tissues and the skeleton. Specific TGF-b family members play different roles in these tissues, and their activities are often balanced with those of other TGF-b family members and by interactions with other signaling pathways. Perturbations in TGF-b family pathways are associated with numerous human diseases with prominent involvement of the skeletal and cardiovascular systems. This review focuses on the role of this family of signaling molecules in the pathologies of connective tissues that manifest in rare genetic syndromes (e.g., syndromic presentations of thoracic aortic aneurysm), as well as in more common disorders (e.g., osteoarthritis and osteoporosis). Many of these diseases are caused by or result in pathological alterations of the complex relationship between the TGF-b family of signaling mediators and the extracellular matrix in connective tissues.T he transforming growth factor b (TGF-b) family of cytokines comprises the three TGF-b proteins (TGF-b1, TGF-b2, and TGFb3) and related growth and differentiation factors such as activins, inhibins, bone morphogenic proteins (BMPs), and growth and differentiation factors (GDFs). These molecules play critical roles both in normal development and in several pathological conditions, including inflammation, fibrosis, and cancer (reviewed in Li and Flavell 2006;Gordon and Blobe 2008;Ikushima and Miyazono 2010). This review focuses on the role of these proteins in development and homeostasis of the skeleton and other connective tissues (summarized in Fig. 1) and on the diseases that ensue when these pathways are altered. Aberrant signaling in these pathways has been associated with common connective 6 These authors contributed equally to this work.

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Cyclic Stretching Stimulates Synthesis of Matrix Components by Arterial Smooth Muscle Cells in Vitro

Cited by 626 publications

References 13 publications

Attenuated Age-Related Carotid Arterial Remodeling in Adults with a High Level of Cardiorespiratory Fitness

Attenuated Age-Related Carotid Arterial Remodeling in Adults with a High Level of Cardiorespiratory Fitness

Biomechanical Determinants of Abdominal Aortic Aneurysm Rupture

TGF-β Family Signaling in Connective Tissue and Skeletal Diseases

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