期刊
NATURE REVIEWS CARDIOLOGY
卷 12, 期 12, 页码 689-710出版社
NATURE PORTFOLIO
DOI: 10.1038/nrcardio.2015.161
关键词
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资金
- Leducq Foundation, Paris, France for the Leducq Mitral Transatlantic Network of Excellence [07CVD04]
- Leducq Foundation Career Development Awards [10CDA01, 11CDA04]
- French Society of Cardiology, Paris, France
- French National Research Agency, Paris, France
- French Ministry of Health, Paris, France
- National Institutes of Health, Bethesda, MD [R01 HL72265, R01 HL109506, R01 HL114805, K24 HL67434, K23 HL116652, R01 HL127692, R01 HL033756, NIGMS P30 GM103342, P20 RR21949, AHA 11SDG5270006]
- Doris Duke Charitable Trust, New York, NY
- Ellison Foundation, Boston, MA
- American Society of Echocardiography, Raleigh, NC
- Austrian Health Ministry Erwin-Schrodinger Fund, Vienna
- Spanish Society of Cardiology, Barcelona
- Eurostars CARDIOMARK Project [E16490]
- European Union, Brussels
- INSERM-DGOS
- Nantes University Translational Research Programs
- Fondation GenaVie, Nantes, France
- French Foundation of Cardiology, Paris, France
- Danish Heart Foundation, Copenhagen
- Fondation de la Recherche Medicale, Paris, France
- Fonds de Recherche du Quebec-Sante, Montreal, Quebec, Canada
- Quebec Office of the Heart and Stroke Foundation, Montreal, Quebec, Canada
- Directorate For Engineering
- Div Of Chem, Bioeng, Env, & Transp Sys [0955172] Funding Source: National Science Foundation
Mitral valve disease is a frequent cause of heart failure and death. Emerging evidence indicates that the mitral valve is not a passive structure, but-even in adult life-remains dynamic and accessible for treatment. This concept motivates efforts to reduce the clinical progression of mitral valve disease through early detection and modification of underlying mechanisms. Discoveries of genetic mutations causing mitral valve elongation and prolapse have revealed that growth factor signalling and cell migration pathways are regulated by structural molecules in ways that can be modified to limit progression from developmental defects to valve degeneration with clinical complications. Mitral valve enlargement can determine left ventricular outflow tract obstruction in hypertrophic cardiomyopathy, and might be stimulated by potentially modifiable biological valvular-ventricular interactions. Mitral valve plasticity also allows adaptive growth in response to ventricular remodelling. However, adverse cellular and mechanobiological processes create relative leaflet deficiency in the ischaemic setting, leading to mitral regurgitation with increased heart failure and mortality. Our approach, which bridges clinicians and basic scientists, enables the correlation of observed disease with cellular and molecular mechanisms, leading to the discovery of new opportunities for improving the natural history of mitral valve disease.
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