alexa Evidence of a Role for Tensile Loading in the Pathogenesis of Mitral Valve Degeneration
ISSN: 2155-9880

Journal of Clinical & Experimental Cardiology
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Review Article

Evidence of a Role for Tensile Loading in the Pathogenesis of Mitral Valve Degeneration

Carla M. R. Lacerda* and E. Christopher Orton
Department of Clinical Sciences, Colorado State University, Fort Collins, Colorado, USA
Corresponding Author : Carla M. R. Lacerda
Department of Clinical Sciences
Colorado State University
Campus Delivery 1678
Fort Collins CO 80523, USA
Tel: 970-297-5010
Fax: 970-297-1275
E-mail: [email protected]
Received November 09, 2011; Accepted January 13, 2012; Published January 16, 2012
Citation: Lacerda CMR, Orton EC (2012) Evidence of a Role for Tensile Loading in the Pathogenesis of Mitral Valve Degeneration. J Clinic Experiment Cardiol S3:004. doi:10.4172/2155-9880.S3-004
Copyright: © 2012 Lacerda CMR, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

Degenerative mitral valve disease (DMVD) is significant cause of cardiovascular morbidity and mortality in humans and dogs. Diseased valves present altered architecture, and distinct pathological characteristics including cell proliferation with phenotype transformation and extracellular matrix turnover with net deposition of proteoglycans, disorganization of collagen and fragmentation elastin. The specific triggers and mediators of leaflet degeneration and chordal rupture are largely unknown. Heart valves are very active tissues, capable of sustaining heavy cyclical loads. Indirect clinical evidence and direct experimental evidence support a hypothesis that DMVD might be initiated by abnormal tensile loading on valvular cells that in turn respond by inappropriate remodeling of the valve matrix. In this review, we present in vivo and in vitro studies linking leaflet or cellular strain to extracellular matrix turnover and expression of myxomatous markers similarly to DMVD. In addition, we discuss additional forces and stimuli that can act as mediators of myxomatous degeneration. Future studies elucidating mechanosensing signaling pathways involved in DMVD will be important to advancing understanding of its pathogenesis.

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