ArticleCardiovascular pathology : the official journal of the Society for Cardiovascular Pathology
Cardiac transgenic matrix metalloproteinase-2 expression induces myxomatous valve degeneration: a potential model of mitral valve prolapse disease.
Article in Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 38 citations in OpenAlex.
- Significance of Fibrillin-1, Filamin A, MMP2 and SOX9 in Mitral Valve Pathology.International journal of molecular sciences · 2024Article
- DZIP1 regulates mammalian cardiac valve development through a Cby1-β-catenin mechanism.Developmental dynamics : an official publication of the American Association of Anatomists · 2021Article
- Biology and Biomechanics of the Heart Valve Extracellular Matrix.Journal of cardiovascular development and disease · 2020Review
- Non-infectious severe aortic regurgitation in a 32-year-old man.BMJ case reports · 2019Article
- Filamin-A as a Balance between Erk/Smad Activities During Cardiac Valve Development.Anatomical record (Hoboken, N.J. : 2007) · 2019Article
- Infectious agents is a risk factor for myxomatous mitral valve degeneration: A case control study.BMC infectious diseases · 2017Observational
- Bisphosphonates in multicentric osteolysis, nodulosis and arthropathy (MONA) spectrum disorder - an alternative therapeutic approach.Scientific reports · 2016Article
- Heart Valve Biomechanics and Underlying Mechanobiology.Comprehensive Physiology · 2016Review
- Mitral valve endothelial cells secrete osteoprotegerin during endothelial mesenchymal transition.Journal of molecular and cellular cardiology · 2016Article
- Current Discoveries and Interventions for Barlow's Disease.Current cardiology reports · 2016Review
- Investigation of the Matrix Metalloproteinase-2 Gene in Patients with Non-Syndromic Mitral Valve Prolapse.Journal of cardiovascular development and disease · 2015Article
- Genetics of valvular heart disease.Current cardiology reports · 2014Review
- Distinct mitral valve proteomic profiles in rheumatic heart disease and myxomatous degeneration.Clinical Medicine Insights. Cardiology · 2014Article
- Article
- Human myxomatous mitral valve prolapse: role of bone morphogenetic protein 4 in valvular interstitial cell activation.Journal of cellular physiology · 2012Article
- A novel intracellular isoform of matrix metalloproteinase-2 induced by oxidative stress activates innate immunity.PloS one · 2012Article
- Cellular mechanisms in mitral valve disease.Journal of cardiovascular translational research · 2011Review
- The transcriptional programme of human heart valves reveals the natural history of infective endocarditis.PloS one · 2010Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
introductionMyxomatous mitral valve "degeneration" with prolapse (MVP) is the most frequent form of nonischemic mitral valve disease. In myxomatous valves, interstitial cells express extracellular matrix-degrading enzymes and it has been postulated that matrix metalloproteinases (MMPs) contribute to these changes.
methodsWe generated mice with cardiac-specific expression of constitutively active MMP-2 under the control of the alpha-myosin heavy chain promoter.
resultsThese mice are normal at 4-6 months of age; at 12-14 months the mitral valves and chordae tendineae exhibit severe myxomatous change with echocardiographic MVP. Myxomatous change was also evident to a lesser extent in the aortic valves. Myxomatous changes were heterogeneous and limited to the left side of the heart with major disorganization of collagen bundles within the lamina fibrosa. Alcian blue/PAS-stained valves revealed massive accumulation of acidic glycosoaminoglycans within the lamina spongiosa, consistent with valvular interstitial cell differentiation to a chondrocytic phenotype. Cells with the histologic features of hypertrophied chondrocytes were found within the chordae tendineae and the tips of the mitral papillary muscles.
conclusionThis report demonstrates that increased activity of a single enzyme, MMP-2, within a transgenic context reproduces many of the features of the human MVP syndrome. The cardiac-specific MMP-2 transgenic mouse potentially provides a unique experimental platform for the evaluation of nonsurgical therapies based on the underlying pathophysiology of this disease.
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