Abstract
Aortic stenosis is the most frequent valvular disease in developed countries. It progresses from mild fibrocalcific leaflet changes to a more severe leaflet calcification at the end stages of the disease. Unfortunately, symptoms of aortic stenosis are unspecific and only appear when it is too late, complicating patients’ management. The global impact of aortic stenosis is increasing due to the growing elderly population. The disease supposes a great challenge because of the multiple comorbidities of these patients. Nowadays, the only effective treatment is valve replacement, which has a high cost in both social and economic terms. For that reason, it is crucial to find potential diagnostic, prognostic and therapeutic indicators that could help us to detect this disease in its earliest stages. In this article, we comprehensively review several key observations and translational studies related to protein markers that are promising for being implemented in the clinical field as well as a discussion about the role of precision medicine in aortic stenosis.
Highlights
Aortic stenosis (AS) is defined as a narrowing of the aortic valve, leading to the obstruction of blood flow from the left ventricle (LV) to the aorta
Genetic factors may be taken into account as genetic polymorphisms and mutations have been associated with AS, including a specific vitamin D receptor allele, which has been correlated with increased risk of AS, neurogenic locus notch homolog protein 1(NOTCH1) mutations in bicuspid aortic valve disease [8]
The results showed that cells treated with either low-density lipoproteins (LDLs) or lipoprotein(a) had significantly higher calcium deposition compared with control cells, pointing to lipoprotein(a) as a potential therapeutic target to manage the progression of AS
Summary
Aortic stenosis (AS) is defined as a narrowing of the aortic valve, leading to the obstruction of blood flow from the left ventricle (LV) to the aorta. The prevalence of aortic valve sclerosis, the precursor to AS, increases significantly with age [2]; about 25% of all 65-year-olds show aortic valve sclerosis, a thickening of the valve without hemodynamic changes [3], and 4–5% have AS [4]. AS has been thought to be a passive degenerative disease, but currently it is known to be an active, complex, and highly regulated pathobiological process involving a multitude of events, such as chronic inflammation, lipoprotein deposition, activation of the renin–angiotensin system, osteoblast differentiation of valvular interstitial cells, and active calcification [5,6]. We consider the mechanisms and pathways implicated for better-targeted treatment, and we highlight the important research efforts to identify biomarkers in AS disease by different techniques, as well as the difficulties found along the way
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