scholarly journals ADAMTS Proteins and Vascular Remodeling in Aortic Aneurysms

Biomolecules ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 12
Author(s):  
Zakaria Mougin ◽  
Julia Huguet Herrero ◽  
Catherine Boileau ◽  
Carine Le Goff

Extracellular matrix (ECM) in the vascular wall is a highly dynamic structure composed of a set of different molecules such as elastins, collagens, fibronectin (Fn), laminins, proteoglycans, and polysaccharides. ECM undergoes remodeling processes to regulate vascular smooth muscle and endothelial cells’ proliferation, differentiation, and adhesion. Abnormalities affecting the ECM can lead to alteration in cellular behavior and from this, this can conduce to the development of pathologies. Metalloproteases play a key role in maintaining the homeostasis of ECM by mediating the cleavage of different ECM components. There are different types of metalloproteases: matrix metalloproteinases (MMPs), disintegrin and metalloproteinases (ADAMs), and ADAMs with thrombospondin motifs (ADAMTSs). ADAMTSs have been found to participate in cardiovascular physiology and diseases and specifically in aortic aneurysms. This review aims to decipher the potential role of ADAMTS proteins in the physiopathologic development of Thoracic Aortic Aneurysms (TAA) and Abdominal Aortic Aneurysms (AAA). This review will focus on what is known on the ADAMTS family involved in human aneurysms from human tissues to mouse models. The recent findings on THSD4 (encoding ADAMTSL6) mutations in TAA give a new insight on the involvement of the ADAMTS family in TAA.

2019 ◽  
Vol 57 ◽  
pp. 210-219 ◽  
Author(s):  
Menno E. Groeneveld ◽  
Joyce A. Struik ◽  
René J.P. Musters ◽  
Geert J. Tangelder ◽  
Pieter Koolwijk ◽  
...  

2015 ◽  
Vol 16 (12) ◽  
pp. 11259-11275 ◽  
Author(s):  
Evan Ryer ◽  
Kaitryn Ronning ◽  
Robert Erdman ◽  
Charles Schworer ◽  
James Elmore ◽  
...  

2013 ◽  
Vol 135 (2) ◽  
Author(s):  
Giampaolo Martufi ◽  
T. Christian Gasser

AAA disease is a serious condition and a multidisciplinary approach including biomechanics is needed to better understand and more effectively treat this disease. A rupture risk assessment is central to the management of AAA patients, and biomechanical simulation is a powerful tool to assist clinical decisions. Central to such a simulation approach is a need for robust and physiologically relevant models. Vascular tissue senses and responds actively to changes in its mechanical environment, a crucial tissue property that might also improve the biomechanical AAA rupture risk assessment. Specifically, constitutive modeling should not only focus on the (passive) interaction of structural components within the vascular wall, but also how cells dynamically maintain such a structure. In this article, after specifying the objectives of an AAA rupture risk assessment, the histology and mechanical properties of AAA tissue, with emphasis on the wall, are reviewed. Then a histomechanical constitutive description of the AAA wall is introduced that specifically accounts for collagen turnover. A test case simulation clearly emphasizes the need for constitutive descriptions that remodels with respect to the mechanical loading state. Finally, remarks regarding modeling of realistic clinical problems and possible future trends conclude the article.


2012 ◽  
Vol 43 (6) ◽  
pp. 1177-1182 ◽  
Author(s):  
Satoshi Yamashiro ◽  
Ryoko Arakaki ◽  
Yuya Kise ◽  
Hitoshi Inafuku ◽  
Yukio Kuniyoshi

2013 ◽  
Vol 2013 ◽  
pp. 1-5 ◽  
Author(s):  
Gianluigi Bisleri ◽  
Lorenzo Bagozzi ◽  
Claudio Muneretto

Thoracic aortic aneurysms have been historically considered to be caused by etiologic factors similar to those implied in abdominal aortic aneurysms. However, during the past decade, there has been increasing evidence that almost 20% of thoracic aortic aneurysms may be associated with a genetic disease, often within a syndromic or familial disorder. Moreover, the presence of congenital anomalies, such as bicuspid aortic valve, may have a unique common genetic underlying cause. Finally, also sporadic forms have been found to be potentially associated with genetic disorders, as highlighted by the analysis of rare variants and expression of specific microRNAs. We therefore sought to perform a comprehensive review of the role of genetic causes in the development of thoracic aortic aneurysms, by analyzing in detail the current evidence of genetic alterations in syndromes such as Marfan, Loeys-Dietz, and Ehler-Danlos, familial or sporadic forms, or forms associated with bicuspid aortic valve.


2015 ◽  
Vol 93 (8) ◽  
pp. 641-648 ◽  
Author(s):  
Azza Ramadan ◽  
Mark D. Wheatcroft ◽  
Adrian Quan ◽  
Krishna K. Singh ◽  
Fina Lovren ◽  
...  

Autophagy regulates cellular homeostasis and integrates the cellular pro-survival machinery. We investigated the role of autophagy in the natural history of murine abdominal aortic aneurysms (AAA). ApoE−/− mice were implanted with saline- or angiotensin II (Ang-II)-filled miniosmotic pumps then treated with either the autophagy inhibitor chloroquine (CQ; 50 mg·(kg body mass)–1·day–1, by intraperitoneal injection) or saline. Ang-II-elicited aneurysmal expansion of the suprarenal aorta coupled with thrombus formation were apparent 8 weeks later. CQ had no impact on the incidence (50% for Ang-II compared with 46.2% for Ang-II + CQ; P = NS) and categorical distribution of aneurysms. The markedly reduced survival rate observed with Ang-II (57.1% for Ang-II compared with 100% for saline; P < 0.05) was unaffected by CQ (61.5% for Ang-II + CQ; P = NS compared with Ang-II). CQ did not affect the mean maximum suprarenal aortic diameter (1.91 ± 0.19 mm for Ang-II compared with 1.97 ± 0.21 mm for Ang-II + CQ; P = NS). Elastin fragmentation, collagen accumulation, and smooth muscle attrition, which were higher in Ang-II-treated mice, were unaffected by CQ treatment. Long-term CQ administration does not affect the natural history and prognosis of experimental AAA, suggesting that global loss of autophagy is unlikely to be a causal factor in the development of aortic aneurysms. Manipulation of autophagy as a mechanism to reduce AAA may need re-evaluation.


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