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Highlights the fibrillin-1/TGF-beta pathway as a key mechanism in the pathogenesis of mitral valve prolapse in Marfan syndrome, offering potential new therapeutic targets.
Mitral valve prolapse (MVP), an abnormal displacement into the left atrium of a thickened and redundant mitral valve during systole, is a relatively frequent abnormality in humans and may be associated with serious complications. A recent study implicates fibrillin-1, a component of extracellular matrix microfibrils, in the pathogenesis of a murine model of MVP. This investigation represents an initial step toward understanding the mechanisms involved in human MVP disease and the development of potential treatments.
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Weyman et al. (2004) studied this question.
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