Key result
High-throughput sequencing of human myxomatous mitral valves provides pathophysiological insights to guide future therapies.
Why the study?
Pathophysiological mechanisms underlying progressive valve leaflet remodeling in myxomatous mitral valve degeneration remain sparsely described, leaving invasive treatments as the only option.
High-throughput sequencing may help elucidate the complex pathophysiological mechanisms of myxomatous mitral valve degeneration to identify novel therapeutic targets.
No immediate clinical application; leaves open validation of sequencing-derived targets in myxomatous mitral valve disease.
Myxomatous mitral valve degeneration (MMVD) is one of the most common valvular heart diseases, affecting 2% to 5% of the general population, and is the main etiology observed in patients with mitral valve prolapse. 1,2 Although MMVD and the subsequent development of mitral valve prolapse/regurgitation are associated with signi fi cant cardiovascular morbidity and mortality, the pathophysiological mechanisms underlying the progressive valve lea fl et remodeling remain only sparsely described, leaving invasive treatments, via surgical or transcatheter approaches, as the only option for patients suffering from severe symptomatic disease. 3 MMVD is characterized by a progressive and heterogeneous thickening of the mitral valve lea fl ets as a consequence of glycosaminoglycan accumulation, with further collagen and elastin fi ber fragmentation. 1,2 These phenotypic traits are the results of complex and interrelated mechanisms mediated by the activation of valvular interstitial cells. 1,2
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Aize et al. (2025) studied this question. High-throughput sequencing of human myxomatous mitral valves provides insights into pathophysiological mechanisms to guide future therapeutic treatments.
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