Key result
Oxidative stress promotes calcific aortic valve disease progression and represents a potential future therapeutic target.
Why the study?
Calcific aortic valve disease has an increasing prevalence and morbidity with no specific pharmacological treatments to date besides aortic valve replacement.
This review highlights the pathophysiological role of oxidative stress in calcific aortic valve disease and its potential as a therapeutic target.
Answers are grounded in this paper and cite their sources.
Supports preclinical exploration of oxidative stress targets in CAVD; leaves open clinical translation without randomized trials.
Calcific aortic valve disease (CAVD) is a major cause of cardiovascular mortality and morbidity, with increased prevalence and incidence. The underlying mechanisms behind CAVD are complex, and are mainly illustrated by inflammation, mechanical stress (which induces prolonged aortic valve endothelial dysfunction), increased oxidative stress (OS) (which trigger fibrosis), and calcification of valve leaflets. To date, besides aortic valve replacement, there are no specific pharmacological treatments for CAVD. In this review, we describe the mechanisms behind aortic valvular disease, the involvement of OS as a fundamental element in disease progression with predilection in AS, and its two most frequent etiologies (calcific aortic valve disease and bicuspid aortic valve); moreover, we highlight the potential of OS as a future therapeutic target.
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Tănase et al. (2022) conducted a review in Calcific aortic valve disease (CAVD). Oxidative stress plays a fundamental role in the progression of calcific aortic valve disease and represents a potential future therapeutic target.
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