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Cited by 386

The DOI matches its Crossref record; 206 of the 206 references it cites were found in a registry or an index.

Mitral valve disease—morphology and mechanisms

Open access
Levine, Robert A., Hagége, Albert A., Judge, Daniel P., Padala, Muralidhar, Dal-Bianco, Jacob P., Aikawa, Elena, Beaudoin, Jonathan, Bischoff, Joyce, Bouatia-Naji, Nabila, Bruneval, Patrick, Butcher, Jonathan T., Carpentier, Alain, Chaput, Miguel, Chester, Adrian H., Clusel, Catherine, Delling, Francesca N., Dietz, Harry C., Dina, Christian, Durst, Ronen, Fernandez-Friera, Leticia, Handschumacher, Mark D., Jensen, Morten O., Jeunemaitre, Xavier P., Marec, Hervé Le, Tourneau, Thierry Le, Markwald, Roger R., Mérot, Jean, Messas, Emmanuel, Milan, David P., Neri, Tui, Norris, Russell A., Peal, David, Perrocheau, Maelle, Probst, Vincent, Pucéat, Michael, Rosenthal, Nadia, Solis, Jorge, Schott, Jean-Jacques, Schwammenthal, Ehud, Slaugenhaupt, Susan A., Song, Jae-Kwan, Yacoub, Magdi H., for the Leducq Mitral Transatlantic Network·2015·Nature Reviews Cardiology

Abstract

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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Crossref · 10.1038/nrcardio.2015.161

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Metadata

Authors
Levine, R. A., Hagége, A. A., Judge, D. P., Padala, M., Dal-Bianco, J. P., Aikawa, E., Beaudoin, J., Bischoff, J., Bouatia-Naji, N., Bruneval, P., Butcher, J. T., Carpentier, A., Chaput, M., Chester, A. H., Clusel, C., Delling, F. N., Dietz, H. C., Dina, C., Durst, R., Fernandez-Friera, L., Handschumacher, M. D., Jensen, M. O., Jeunemaitre, X. P., Marec, H. L., Tourneau, T. L., Markwald, R. R., Mérot, J., Messas, E., Milan, D. P., Neri, T., Norris, R. A., Peal, D., Perrocheau, M., Probst, V., Pucéat, M., Rosenthal, N., Solis, J., Schott, J.-J., Schwammenthal, E., Slaugenhaupt, S. A., Song, J.-K., Yacoub, M. H., & for the Leducq Mitral Transatlantic Network
Venue
Nature Reviews Cardiology
Published
2015-10-20
Volume
12
Issue
12
Pages
689-710
ISSN
  • 1759-5002 (ISSN-L)
  • 1759-5010
OpenAlex
W1754892555
Cited by
386
References
206
FWCI
5.88
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Mitral valve disease—morphology and mechanisms. https://app.cochat.ai/papers/10.1038/nrcardio.2015.161
The paper
Levine, R. A., Hagége, A. A., Judge, D. P., Padala, M., Dal-Bianco, J. P., Aikawa, E., Beaudoin, J., Bischoff, J., Bouatia-Naji, N., Bruneval, P., Butcher, J. T., Carpentier, A., Chaput, M., Chester, A. H., Clusel, C., Delling, F. N., Dietz, H. C., Dina, C., Durst, R., . . . for the Leducq Mitral Transatlantic Network. (2015). Mitral valve disease—morphology and mechanisms. Nature Reviews Cardiology. https://doi.org/10.1038/nrcardio.2015.161

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.