Mitral valve prolapse (MVP) represents a common degenerative disease, often requiring surgery. If untreated, MVP with considerable valve incompetence can lead to cardiovascular and systemic complications causing substantial morbidity and mortality. In contrast with the wide knowledge concerning clinical and physiological features, currently available data regarding its molecular bases are very limited. We review current knowledge concerning MVP biological mechanisms, focusing on specific aspects of haemostasis, platelet function, oxidative stress, extracellular matrix remodeling and genomics. In particular, available evidence supports the role played by tissue remodeling processes in determining MVP onset and progression. Moreover, even if a consistent although controversial perturbation of haemostatic system and alterations of the oxidative stress equilibrium have been proposed to influence disease development, it is unknown whether these changes precede or follow MVP occurrence. Consequently, the complete knowledge of all the biochemical pathways involved are far from complete. In addition, changes in the regulation pattern of adrenergic and renin-angiotensin-aldosterone systems have been described in MVP syndrome, a condition characterized by the association of MVP with other peculiar neurological and general symptoms, but it is unknown whether these abnormalities are shared by "traditional" MVP. In conclusion, MVP is probably a multi-factorial process, and many aspects still need to be clarified. As surgery can only correct the damaged valve but not the underlying mechanisms, a more complete knowledge of the involved molecular pathways is necessary, as it may allow the discovery of targeted therapeutic strategies aimed at modifying or slackening MVP natural course in the early phases.
- Extracellular matrix
- Mitral valve prolapse
- Mitral valve prolapse syndrome
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine