Collagen stability and collagenolytic activity in the normal and aneurysmal human abdominal aorta

Webster, Marshall W.; McAuley, Clyde E.; Steed, David L.; Miller, David D.; Evans, Christopher H.

doi:10.1016/0002-9610(91)91246-f

Cited by 25 publications

(7 citation statements)

References 21 publications

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“…It appears to be more active against immature or damaged collagen. Collagenase is synthesized as a latent proenzyme, and is activated in its precursor procollagenase form by stromelysin, which is produced endogenously within the aorta [46]. It can also be activated by proteinases or organomercurials, 4-aminophenylmercuric acetate (APMA), plasmin, or trypsin [103,104].…”

Section: Enzymatic Degradationmentioning

confidence: 99%

“…These findings would appear to confirm an ongoing but ineffective elastogenesis by smooth muscle cells and macrophages. This impairment in the integration of new collagen and elastin fibers may severely compromise the integrity and biomechanical properties of the arterial wall, and renders these components more susceptible to further enzymatic degradation [45,46].…”

Section: Introductionmentioning

confidence: 99%

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The pathobiology of aortic aneurysms

Alexander

2004

Journal of Surgical Research

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Section: Enzymatic Degradationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The pathobiology of aortic aneurysms

Alexander

2004

Journal of Surgical Research

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“…Collagen is produced by fibre-producing cells such as fibroblasts and smooth muscle cells, and collagen degradation is accomplished by collagenases (Dobrin and Canfield, 1984;Murphy and Reynolds, 1985). Increased levels of collagenases have also been observed in aneurysmal tissue (AAssar et al, 2003;Anidjar et al, 1992;McMillan et al, 1995;Sluijter et al, 2004;Webster et al, 1991). The production of collagen (Type I) in cerebral aneurysms is mainly accomplished by fibroblasts (Eastwood et al, 1998;Espinosa et al, 1984;Kamphorst et al, 1991;Sluijter et al, 2004;Tóth et al, 1998), and these cells therefore play a key role in aneurysmal growth.…”

mentioning

confidence: 99%

A theoretical model for fibroblast-controlled growth of saccular cerebral aneurysms

Kroon

Holzapfel

2009

Journal of Theoretical Biology

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A new theoretical model for the growth of saccular cerebral aneurysms is proposed by extending the recent constitutive framework of Kroon and Holzapfel (J. Theor. Biol., 247:775-787, 2007). The continuous turnover of collagen is taken to be the driving mechanism in aneurysmal growth. The collagen production rate depends on the magnitude of the cyclic deformation of fibroblasts, caused by the pulsating blood pressure during the cardiac cycle. The volume density of fibroblasts in the aneurysmal tissue is taken to be constant throughout the growth process. The growth model is assessed by considering the inflation of an axisymmetric membranous piece of aneurysmal tissue, with material characteristics representative of a cerebral aneurysm. The diastolic and systolic states of the aneurysm are computed, together with its load-free state. It turns out that the value of collagen pre-stretch, that determines growth speed and stability of the aneurysm, is of pivotal importance. The model is able to predict aneurysms with typical berry-like shapes observed clinically, and the predicted wall stresses correlate well with the experimentally obtained ultimate stresses of this type of tissue. The model predicts that aneurysms should fail when reaching a size of about 1.2-3.6 mm, which is smaller than what has been clinically observed. With some refinements, the model may, however, be used to predict future growth of diagnosed aneurysms.

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“…22- 25 The elastin and collagen degradation in the aneurysm wall is contributed by the matrix metalloproteinase (MMP) family such as collagenase-1 (MMP-1), stromelysin-1 (MMP-3), the 72-kDa gelatinase (MMP-2) and the 92-kDa gelatinase (MMP-9), macrophage elastase (MMP-12) and collagenase-3 (MMP13). 22,23,[26][27][28][29] MMPs are structurally related metalloendopeptidases that can degrade the extracellular matrix and play important roles in normal tissue development and remodeling. Abnormal expression of MMPs is associated with various pathological processes such as osteoarthritis, rheumatoid arthritis, tumor invasion and metastasis, pulmonary emphysema and atherosclerosis.…”

Section: Etiology and Pathogenesis Of Aaamentioning

confidence: 99%

Current Status of Medical Treatment for Abdominal Aortic Aneurysm

Kurosawa

Matsumura

Yamanouchi

2013

Circ J

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Circulation Journal Official Journal of the Japanese Circulation Society http://www. j-circ.or.jp bdominal aortic aneurysm (AAA) is a common condition of increasing prevalence, particularly among older men. 1,2 Aneurysm-related mortality is responsible for approximately 15,000 deaths in 2010 in the USA. 1, 3 Although there are approximately 55,000 patients who undergo AAA repairs annually, the overall incidence of AAA is probably estimated to be higher. 4 AAA occurs in 4-9% of the population over the age of 65 years according to the screening studies, and affects approximately 1.7 million individuals 5-8 in the USA.Many groups have researched the pathophysiology of AAA with the intent to discover an effective medical treatment through a biological or molecular approach. 9-15 Matrix metalloproteinase (MMP) is a key proteinase mechanism in the development and growth of AAA. Effective medical treatment for AAA has not been established yet; however, it would be beneficial to avoid the invasive interventions and it would be expected to reduce the medical cost. 1, 16 We reviewed the current treatment options and potential medical treatment for AAA. Etiology and Pathogenesis of AAAAAA is hypothesized to be caused by multifunctional degenerative processes, including extracellular matrix remodeling, vascular smooth muscle cell apoptosis/necrosis, oxidative stress and infiltration of inflammatory cells. Genetic disorder, inflammation, infection and connective tissue disease are also causal underlying factors of destructive degeneration of the aortic wall. 17-21 While the precise etiology of AAA hasn't been fully understood yet, it is certain that the progression of aneurysmal degeneration involves destructive remodeling of the aneurysmal wall.Elastin is the one of the key structural proteins of extracellular matrix in the aortic wall and maintains the integrity of the wall. Numerous studies suggest that proteolytic degradation of elastin in the medial layer leads to weakening and dilatation of the aortic wall while collagen degradation accounts for the rupture of the aneurysm. 22-25 The elastin and collagen degradation in the aneurysm wall is contributed by the matrix metalloproteinase (MMP) family such as collagenase-1 (MMP-1), stromelysin-1 (MMP-3), the 72-kDa gelatinase (MMP-2) and the 92-kDa gelatinase (MMP-9), macrophage elastase (MMP-12) and collagenase-3 (MMP13). 22,23,26-29MMPs are structurally related metalloendopeptidases that can degrade the extracellular matrix and play important roles in normal tissue development and remodeling. Abnormal expression of MMPs is associated with various pathological processes such as osteoarthritis, rheumatoid arthritis, tumor invasion and metastasis, pulmonary emphysema and atherosclerosis. 30-34 Regulation of MMP activities has been attempted (to prevent the tissue degradation) by controlling them at different levels of the activation processes. The tissue inhibitor of metalloproteinases (TIMPs) are physiological inhibitors of MMP activity. Several studies suggested that aneury...

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Collagen stability and collagenolytic activity in the normal and aneurysmal human abdominal aorta

Cited by 25 publications

References 21 publications

The pathobiology of aortic aneurysms

The pathobiology of aortic aneurysms

A theoretical model for fibroblast-controlled growth of saccular cerebral aneurysms

Current Status of Medical Treatment for Abdominal Aortic Aneurysm

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