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Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling
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[The role of transforming growth factor-β in the pathogenesis of mitral valve prolapse]

E G Malev, E V Zemtsovskiĭ, M Iu Omel'chenko

    Kardiologiia
    |December 15, 2012
    PubMed

    Insights

    High levels of Transforming Growth Factor-beta (TGF-β) are linked to mitral valve prolapse progression and reduced left ventricular function in patients with myxomatous degeneration.

    Area of Science:

    • Cardiovascular Biology
    • Molecular Medicine
    • Connective Tissue Disorders

    Background:

    • Transforming Growth Factor-beta (TGF-β) signaling pathway alterations are implicated in inherited connective tissue disorders.
    • The specific role of TGF-β in mitral valve prolapse (MVP) pathogenesis remains incompletely understood.

    Purpose of the Study:

    • To investigate the association between TGF-β activity and the structural and functional characteristics of the mitral valve in patients with MVP.
    • To evaluate the impact of elevated TGF-β levels on left ventricular (LV) function in MVP patients.

    Main Methods:

    • Analysis of 35 patients undergoing reconstructive surgery for MVP with severe mitral insufficiency.
    • Measurement of TGF-β1/2 levels in patient samples.
    • Correlation analysis between TGF-β levels, mitral valve leaflet thickness, residual prolapse, mitral regurgitation, and LV strain (systolic and diastolic) and strain rate (SR).

    Main Results:

    • Elevated TGF-β1/2 levels were detected in 65% of patients.
    • High TGF-β1/2 correlated significantly with increased posterior leaflet thickness, residual valve prolapse, and residual mitral regurgitation.
    • Patients with high TGF-β1/2 exhibited significantly reduced LV longitudinal systolic and diastolic strain and SR, suggesting impaired cardiac function.

    Conclusions:

    • TGF-β plays a significant role in the progression of myxomatous degeneration of the mitral valve.
    • Increased TGF-β signaling activity contributes to reduced left ventricular function, likely through profibrotic mechanisms.

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