scholarly journals iTRAQ proteomic analysis of extracellular matrix remodeling in aortic valve disease

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Tatiana Martin-Rojas ◽  
Laura Mourino-Alvarez ◽  
Sergio Alonso-Orgaz ◽  
Esther Rosello-Lleti ◽  
Enrique Calvo ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Aortic Valve ◽  
Proteomic Analysis ◽  
Aortic Valve Disease ◽  
Valve Disease ◽  
Extracellular Matrix Remodeling ◽  
Matrix Remodeling

scholarly journals Identification of key genes in calcific aortic valve disease via weighted gene co-expression network analysis

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Jin-Yu Sun ◽  
Yang Hua ◽  
Hui Shen ◽  
Qiang Qu ◽  
Jun-Yan Kan ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Network Analysis ◽  
Aortic Valve ◽  
Aortic Valve Disease ◽  
Expression Profiles ◽  
Enrichment Analysis ◽  
Valve Disease ◽  
Hub Genes ◽  
Calcific Aortic Valve Disease ◽  
Underlying Mechanisms

Abstract Background Calcific aortic valve disease (CAVD) is the most common subclass of valve heart disease in the elderly population and a primary cause of aortic valve stenosis. However, the underlying mechanisms remain unclear. Methods The gene expression profiles of GSE83453, GSE51472, and GSE12644 were analyzed by ‘limma’ and ‘weighted gene co-expression network analysis (WGCNA)’ package in R to identify differentially expressed genes (DEGs) and key modules associated with CAVD, respectively. Then, enrichment analysis was performed based on Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway, DisGeNET, and TRRUST database. Protein–protein interaction network was constructed using the overlapped genes of DEGs and key modules, and we identified the top 5 hub genes by mixed character calculation. Results We identified the blue and yellow modules as the key modules. Enrichment analysis showed that leukocyte migration, extracellular matrix, and extracellular matrix structural constituent were significantly enriched. SPP1, TNC, SCG2, FAM20A, and CD52 were identified as hub genes, and their expression levels in calcified or normal aortic valve samples were illustrated, respectively. Conclusions This study suggested that SPP1, TNC, SCG2, FAM20A, and CD52 might be hub genes associated with CAVD. Further studies are required to elucidate the underlying mechanisms and provide potential therapeutic targets.

scholarly journals Extracellular matrix remodelling in human aortic valve disease: the role of matrix metalloproteinases and their tissue inhibitors

2005 ◽  
Vol 26 (13) ◽  
pp. 1333-1341 ◽  
Author(s):  
Olivier Fondard ◽  
Delphine Detaint ◽  
Bernard Iung ◽  
Christine Choqueux ◽  
Homa Adle-Biassette ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Aortic Valve ◽  
Matrix Metalloproteinases ◽  
Aortic Valve Disease ◽  
Valve Disease ◽  
Tissue Inhibitors ◽  
Extracellular Matrix Remodelling ◽  
Human Aortic Valve

scholarly journals Maladaptive matrix remodeling and regional biomechanical dysfunction in a mouse model of aortic valve disease

2012 ◽  
Vol 31 (3) ◽  
pp. 197-205 ◽  
Author(s):  
Varun K. Krishnamurthy ◽  
Amy M. Opoka ◽  
Christine B. Kern ◽  
Farshid Guilak ◽  
Daria A. Narmoneva ◽  
...  
Keyword(s):  
Aortic Valve ◽  
Mouse Model ◽  
Aortic Valve Disease ◽  
Valve Disease ◽  
Matrix Remodeling

scholarly journals Decellularization of rat aortic valve allografts reduces leaflet destruction and extracellular matrix remodeling

2003 ◽  
Vol 126 (6) ◽  
pp. 2003-2010 ◽  
Author(s):  
R.W Grauss ◽  
M.G Hazekamp ◽  
S van Vliet ◽  
A.C Gittenberger-de Groot ◽  
M.C DeRuiter
Keyword(s):  
Extracellular Matrix ◽  
Aortic Valve ◽  
Extracellular Matrix Remodeling ◽  
Matrix Remodeling

scholarly journals Extracellular Matrix in Calcific Aortic Valve Disease: Architecture, Dynamic and Perspectives

2021 ◽  
Vol 22 (2) ◽  
pp. 913
Author(s):  
Anna Di Vito ◽  
Annalidia Donato ◽  
Ivan Presta ◽  
Teresa Mancuso ◽  
Francesco Saverio Brunetti ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Aortic Valve ◽  
Aortic Valve Disease ◽  
Matrix Vesicles ◽  
Developed Countries ◽  
Valve Disease ◽  
Ageing Population ◽  
Calcific Aortic Valve Disease ◽  
Molecular Alterations ◽  
Active Processes

Calcific Aortic Valve Disease (CAVD) is the most common valvular heart disease in developed countries and in the ageing population. It is strongly correlated to median age, affecting up to 13% of the population over the age of 65. Pathophysiological analysis indicates CAVD as a result of an active and degenerative disease, starting with sclerosis and chronic inflammation and then leaflet calcification, which ultimately can account for aortic stenosis. Although CAVD has been firstly recognized as a passive event mostly resulting from a degenerative aging process, much evidences suggests that calcification arises from different active processes, involving both aortic valve-resident cells (valve endothelial cells, valve interstitial cells, mesenchymal stem cells, innate immunity cells) and circulating cells (circulating mesenchymal cells, immunity cells). Moreover, a role for the cell-derived “matrix vesicles” and extracellular matrix (ECM) components has also been recognized. The aim of this work is to review the cellular and molecular alterations occurring in aortic valve during CAVD pathogenesis, focusing on the role of ECM in the natural course of the disease.

scholarly journals Matrix remodeling in human aortic valve disease

2003 ◽  
Vol 41 (6) ◽  
pp. 508 ◽  
Author(s):  
Olivier Fondard ◽  
Delphine Detaint ◽  
Homa Adle ◽  
Bernard lung ◽  
Jean-Paul Couetil ◽  
...  
Keyword(s):  
Aortic Valve ◽  
Aortic Valve Disease ◽  
Valve Disease ◽  
Matrix Remodeling ◽  
Human Aortic Valve

scholarly journals Cadherin-11 coordinates cellular migration and extracellular matrix remodeling during aortic valve maturation

2015 ◽  
Vol 407 (1) ◽  
pp. 145-157 ◽  
Author(s):  
Caitlin J. Bowen ◽  
Jingjing Zhou ◽  
Derek C. Sung ◽  
Jonathan T. Butcher
Keyword(s):  
Extracellular Matrix ◽  
Aortic Valve ◽  
Cellular Migration ◽  
Extracellular Matrix Remodeling ◽  
Matrix Remodeling

scholarly journals Pathogenesis and Molecular Immune Mechanism of Calcified Aortic Valve Disease

2021 ◽  
Vol 8 ◽  
Author(s):  
Weikang Bian ◽  
Zhicheng Wang ◽  
Chongxiu Sun ◽  
Dai-Min Zhang
Keyword(s):  
Aortic Valve ◽  
Aortic Valve Disease ◽  
Valve Disease ◽  
Calcium Deposition ◽  
Matrix Remodeling ◽  
Future Directions ◽  
Transcatheter Aortic Valve ◽  
New Ideas ◽  
Valve Implantation ◽  
Insight Into

Calcified aortic valve disease (CAVD) was previously regarded as a passive process associated with valve degeneration and calcium deposition. However, recent studies have shown that the occurrence of CAVD is an active process involving complex changes such as endothelial injury, chronic inflammation, matrix remodeling, and neovascularization. CAVD is the ectopic accumulation of calcium nodules on the surface of the aortic valve, which leads to aortic valve thickening, functional stenosis, and ultimately hemodynamic disorders. CAVD has become an important cause of death from cardiovascular disease. The discovery of therapeutic targets to delay or block the progression of CAVD and the clinical application of transcatheter aortic valve implantation (TAVI) provide new ideas for the prevention and treatment of CAVD. This article summarizes the pathogenesis of CAVD and provides insight into the future directions of CAVD diagnosis and treatment.

scholarly journals Dissecting Calcific Aortic Valve Disease—The Role, Etiology, and Drivers of Valvular Fibrosis

2021 ◽  
Vol 8 ◽  
Author(s):  
Petra Büttner ◽  
Lukas Feistner ◽  
Philipp Lurz ◽  
Holger Thiele ◽  
Joshua D. Hutcheson ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Aortic Valve ◽  
Aortic Valve Disease ◽  
Molecular Mechanisms ◽  
Left Ventricular ◽  
Valve Disease ◽  
Reverse Remodeling ◽  
Calcific Aortic Valve Disease ◽  
Ecm Remodeling ◽  
The Individual

Calcific aortic valve disease (CAVD) is a highly prevalent and progressive disorder that ultimately causes gradual narrowing of the left ventricular outflow orifice with ensuing devastating hemodynamic effects on the heart. Calcific mineral accumulation is the hallmark pathology defining this process; however, fibrotic extracellular matrix (ECM) remodeling that leads to extensive deposition of fibrous connective tissue and distortion of the valvular microarchitecture similarly has major biomechanical and functional consequences for heart valve function. Significant advances have been made to unravel the complex mechanisms that govern these active, cell-mediated processes, yet the interplay between fibrosis and calcification and the individual contribution to progressive extracellular matrix stiffening require further clarification. Specifically, we discuss (1) the valvular biomechanics and layered ECM composition, (2) patterns in the cellular contribution, temporal onset, and risk factors for valvular fibrosis, (3) imaging valvular fibrosis, (4) biomechanical implications of valvular fibrosis, and (5) molecular mechanisms promoting fibrotic tissue remodeling and the possibility of reverse remodeling. This review explores our current understanding of the cellular and molecular drivers of fibrogenesis and the pathophysiological role of fibrosis in CAVD.

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