Expression of uPA, tPA, and PAI-1 in Calcified Aortic Valves.

Purpose. Our physiopathological assumption is that u-PA, t-PA, and PAI-1 are released by calcified aortic valves and play a role in the calcification of these valves. Methods.

Release of leukotriene B4, transforming growth factor-beta1 and microparticles in relation to aortic valve calcification.

Background And Aim Of The Study: Aortic stenosis, the most frequent valvulopathy in the Western world, is characterized by an important extracellular matrix (ECM) remodeling and a process of calcification in the aortic valves. One physiopathological assumption is that transforming growth factor-beta1 (TGF-beta1) acts through ECM remodeling and plays a role in calcification, implicating also microparticles (MPs). Another recent notion is the active involvement of inflammatory mediators in the calcification process of aortic stenosis.

[Aortic stenosis and extracellular matrix remodeling].

Valvular heart diseases represent an important public health burden. With the decrease in the incidence of rheumatic heart disease, calcific aortic stenosis has now become the most common valvular disease in Western countries. Its prevalence increases with age, such that its affects about 4% of the elderly population and it is the most common motive for valve replacement.

Plasmin induces apoptosis of aortic valvular myofibroblasts.

Previous studies have described remodelling of the extracellular substratum by matrix metalloproteinases (MMPs) in aortic valves. However, involvement of the fibrinolytic system has not yet been analysed. We hypothesized that plasminogen and plasminogen activator(s) are present in aortic valves and that plasminogen activation could induce the degradation of adhesive proteins and apoptosis of the valvular myofibroblasts.