Elastin and collagen fibre microstructure of the human aorta in ageing and disease: a review

Tsamis, Alkiviadis; Krawiec, Jeffrey T.; Vorp, David A.

doi:10.1098/rsif.2012.1004

Cited by 405 publications

(328 citation statements)

References 124 publications

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“…As shown in the presented results, degradation of the elastin fibers was observed in the MFS and TAA tissue, also consistent with previously published findings (32)(33)(34). In addition to elastin degradation, higher interfibrillar spaces, and decreased elastin fiber concentration have been documented (32)(33)(34), supporting our results.…”

Section: Structuresupporting

confidence: 82%

“…In addition to elastin degradation, higher interfibrillar spaces, and decreased elastin fiber concentration have been documented (32)(33)(34), supporting our results. Collagen fiber composition and concentration were not found to be affected in the TAA and MFS conditions (33,35); however, studies also show increased rates of collagen synthesis and turnover in MFS patients (34). These results also agree with our findings, as evidenced by the observed increase of newer, thinner collagen in the MFS groups as compared to the TAA and the age-matched healthy controls.…”

Section: Structuresupporting

confidence: 81%

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Biomechanical properties of the thoracic aorta in Marfan patients

Sulejmani¹,

Pokutta-Paskaleva²,

Ziganshin³

et al. 2017

Ann. Cardiothorac. Surg.

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Background: Marfan syndrome (MFS), a genetic disorder of the connective tissue, has been strongly linked to dilation of the thoracic aorta, among other cardiovascular complications. As a result, MFS patients frequently suffer from aortic dissection and rupture, contributing to the high rate of mortality and morbidity among MFS patients. Despite the significant effort devoted to the investigation of mechanical and structural properties of aneurysmal tissue, studies on Marfan aneurysmal biomechanics are scarce. Ex vivo mechanical characterization of MFS aneurysmal tissue can provide a better insight into tissue strength outside the physiologic loading range and serve as a basis for improved risk assessment and failure prediction. Methods:The mechanical and microstructural properties of MFS aneurysmal thoracic aorta (MFS, n=15, 39.5±3.91 years), non-MFS aneurysmal thoracic aorta (TAA, n=8, 52.8±4.9 years), healthy human thoracic aorta (HH, n=8, 75.4±6.1 years), and porcine thoracic aorta (n=10) are investigated. Planar biaxial tensile testing and uniaxial failure testing were utilized to characterize the mechanical and failure properties of the tissue, respectively. Verhoeff-Van Gieson (VVG) and PicroSirius Red stains were utilized to visualize the elastin and collagen fiber architecture, respectively.Results: MFS tissue was found to have age-dependent but diameter-independent mechanical, structural, and morphological properties, also showing extensive elastin fiber degradation. Non-MFS thoracic aneurysmal aorta was thicker and stiffer than age-matched MFS tissue. Moreover, non-MFS thoracic aneurysmal mechanics resembled closely the mechanics of older healthy human tissue. Younger MFS tissue (<40 years) exhibited similar mechanical and structural properties to aged porcine tissue.Conclusions: Both age and aneurysmal presence were found to be factors associated with increased stiffness in aortic tissue, and aortic diameter was not a significant determinant of mechanical property deterioration. Additionally, the presence of MFS was found to induce stiffening of the thoracic aorta, although not to the extent of the non-MFS aneurysm.

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Section: Structuresupporting

confidence: 82%

Section: Structuresupporting

confidence: 81%

Biomechanical properties of the thoracic aorta in Marfan patients

Sulejmani¹,

Pokutta-Paskaleva²,

Ziganshin³

et al. 2017

Ann. Cardiothorac. Surg.

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“…(Horgan and Saccomandi, 2003;Li and Robertson, 2009;Tsamis et al, 2013), damage and remodeling (Ferrara and Pandolfi, 2008;Ni Annaidh et al, 2012;Sánchez et al, 2014). As a consequence of the intrinsically patient-specific nature and of the microstructural complexity of biological tissues, their modeling is very challenging and still incomplete.…”

Section: Introductionmentioning

confidence: 99%

Statistical characterization of the anisotropic strain energy in soft materials with distributed fibers

Gizzi

Pandolfi

Vasta

2016

Mechanics of Materials

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a b s t r a c tWe discuss analytical and numerical tools for the statistical characterization of the anisotropic strain energy density of soft hyperelastic materials embedded with fibers. We consider spatially distributed orientations of fibers following a tridimensional or a planar architecture. We restrict our analysis to material models dependent on the fourth pseudo-invariant I 4 of the Cauchy-Green tensor, and to exponential forms of the fiber strain energy function aniso . Under different loading conditions, we derive the closed-form expression of the probability density function for I 4 and aniso . In view of bypassing the cumbersome extension-contraction switch, commonly adopted for shutting down the contribution of contracted fibers in models based on generalized structure tensors, for significant loading conditions we identify analytically the support of the fibers in pure extension. For uniaxial loadings, the availability of the probability distribution function and the knowledge of the support of the fibers in extension yield to the analytical expression of average and variance of I 4 and aniso , and to the direct definition of the average second Piola-Kirchhoff stress tensor. For generalized loadings, the dependence of I 4 on the spatial orientation of the fibers can be analyzed through angle plane diagrams. Angle plane diagrams facilitate the assessment of the influence of the pure extension condition on the definition of the stable support of fibers for the statistics related to the anisotropic strain energy density.

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“…However, GWASs were performed using only known genetic markers involved in both cases and healthy controls, the ability to identify novel pathogenesis is limited compared with direct sequencing (Marian and Belmont, 2011;Salomon et al, 2016). It is clear that the imbalance of the homeostasis between collagens and MMPs/TIMPs system is a key responsible for extracellular matrix (ECM) degeneration and structure and functions of aorta, and therefore may contribute to the pathogenesis of AD (Barbour et al, 2007;Theruvath et al, 2012;Tsamis et al, 2013). However, to date, except for gene COL3A1, no pathogenic genes in collagens and MMP/TIMPs system have been demonstrated in AD patients (Sakai et al, 2012;Smith et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Variants of genes encoding collagens and matrix metalloproteinase system increased the risk of aortic dissection

Zhou

Tan

et al. 2016

Sci. China Life Sci.

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Aortic dissection (AD) is a devastating, heterogeneous condition of aorta. The homeostasis between collagens and matrix metalloproteases (MMPs)/tissue inhibitors of MMPs (TIMPs) system in the extracellular matrix plays an important role for structure and functions of aorta. However, our knowledge on association between variants of genes in this system and pathogenesis of AD is very limited. We analyzed all yet known coding human genes of collagens (45 genes), MMPs/TIMPs (27 genes) in 702 sporadic AD patients and in 163 matched healthy controls, by using massively targeted next-generation and Sanger sequencing. To define the pathogenesis of potential disease-causing candidate genes, we performed transcriptome sequencing and pedigree co-segregation analysis in some genes and generated Col5a2 knockout rats. We identified 257 pathogenic or likely pathogenic variants which involved 88.89% (64/72) genes in collagens-MMPs/TIMPs system and accounted for 31.05% (218/702) sporadic AD patients. In them, 84.86% patients (185/218) carried one variant, 12.84% two variants and 2.30% more than two variants. Importantly, we identified 52 novel probably pathogenic loss-of-function (LOF) variants (20 nonsense, 16 frameshift, 14 splice sites, one stop-loss, one initiation codon) in 11.06% (50/452) AD patients, which were absent in 163 controls (P=2.5×10 −5 ). Transcriptome sequencing revealed that identified variants induced dyshomeostasis in expression of collagens-TIMPs/MMPs systems. The Col5a2 −/− rats manifested growth retardation and aortic dysplasia. Our study provides a first comprehensive map of genetic alterations in collagens-MMPs/TIMPs system in sporadic AD patients and suggests that variants of these genes contribute largely to AD pathogenesis. aortic dissection, collagen, matrix metalloproteinase, next-generation sequencing, genetic diagnosis Citation:Li, Z., Zhou, C., Tan, L., Chen, P., Cao, Y., Li, C., Li, X., Yan, J., Zeng, H., Wang, D.W., and Wang, D.W. (2017). Variants of genes encoding collagens and matrix metalloproteinase system increased the risk of aortic dissec. Sci China Life Sci 60, 57-65.

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Elastin and collagen fibre microstructure of the human aorta in ageing and disease: a review

Cited by 405 publications

References 124 publications

Biomechanical properties of the thoracic aorta in Marfan patients

Biomechanical properties of the thoracic aorta in Marfan patients

Statistical characterization of the anisotropic strain energy in soft materials with distributed fibers

Variants of genes encoding collagens and matrix metalloproteinase system increased the risk of aortic dissection

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