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Mitral valve prolapse (MVP) is defined as the systolic displacement of one or both mitral leaflets into the left atrium. Glaucoma is a neurodegenerative disease characterised by elevated intraocular pressure (IOP), with typical slow, progressive degeneration of retinal ganglion cells and optic-nerve cupping. In primary open-angle glaucoma (OAG), the predominant form of glaucoma in Western countries, the iridocorneal angle is open and normal in appearance but aqueous humour outflow is diminished. How can an association between MVP and OAG even be postulated? Indeed, the two conditions share multiple common features, from a similar prevalence in the general population (approximately 3%)1 ,2 to the potential for significant adverse clinical outcomes (heart failure, need for surgery, sudden cardiac death in MVP and blindness in OAG).1 ,2 Most importantly, myxomatous degeneration is found histologically in prolapsing mitral leaflets in MVP, and in the trabecular meshwork of the iris and the ciliary body in OAG.1 ,3
Extracellular matrix abnormalities in MVP and OAG
The extracellular matrix (ECM) constitutes the fibroskeleton of a normal mitral valve and the normal trabecular meshwork in the eye. Valvular leaflets are populated on the surface by endothelial cells and by interstitial cells (VICs) within the valve.1 Quiescent VICs are non-contractile, fibroblast-like cells that can synthesise and degrade matrix enzymes. Enzymes secreted by VICs include matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs (TIMPs).1 Quiescent VICs maintain a tight balance between degradation and synthesis of the matrix proteins, thus allowing normal valve leaflet strength and function. Myxomatous degeneration is characterised by the accumulation of proteoglycans and consequent expansion of the middle spongiosa layer of the valve, and structural alterations of collagen in all components of the valve leaflet. Dysregulation of ECM components plays a key role in mediating these changes. In MVP, VICs acquire properties of activated myofibroblasts responsible …
Contributors FND and RSV contributed to this editorial.
Funding This work was supported by the National Heart, Lung and Blood Institute (NHLBI) research grant K23HL116652 (FND) and in part by the NHLBI contract N01-HC-25195 (RSV).
Competing interests None.
Provenance and peer review Commissioned; internally peer reviewed.
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