Title:Understanding the Molecular and Cellular Changes Behind Aortic Valve Stenosis
Volume: 13
Issue: 13
Author(s): Ines Falcao-Pires, Cristina Gavina and Adelino F. Leite-Moreira
Affiliation:
Keywords:
Aortic stenosis, aortic valve, myocardium, pressure overload
Abstract: Morbidity from degenerative aortic valve disease (AVS) is increasing worldwide, concomitant with the ageing
of the population and the growing consumption of high caloric and cholesterol diets of the western countries. Despite the
increasing prevalence of AVS, with its high mortality and morbidity, studies on the molecular and cellular mechanisms
underlying the onset of aortic valve degeneration have only advanced in the last 15 years. The result of this effort is now
beginning to reveal several mechanisms with great therapeutic targeting potential that may alter the natural history of this
progressive pathology. Indeed, the view of this disease has changed from being an unmodifiable degenerative disease to
an active biological process regulated by highly conserved cellular pathways. The progression of AVS includes inflammation,
angiogenesis and remodelling of the extracellular matrix leading to osteogenesis in the aortic valve and revealing
many mechanisms and risk factors similar to atherosclerosis. Therefore statins and angiotensin II antagonists seemed
promising treatment options; however, experimental results are still controversial. Nonetheless, valvular degeneration results
in dramatic myocardial changes induced by chronic pressure overload such as left ventricular hypertrophy as well as
other paramount myocardial extracellular changes. Currently, a strong impulse for future research to investigate the
pathophysiological mechanisms and their modulation in order to prevent/delay the onset or progression of valve degeneration
is needed. In the present review, we focused on the molecular and cellular mechanisms underlying degenerative AVS
and its myocardial impact.
