Key result
The pathogenesis of calcific aortic valve disease involves oxidized lipoprotein deposition and inflammation in the initiation phase, and active ectopic calcification in the progression phase.
Why the study?
Calcific aortic valve disease has an unfavorable prognosis and lacks effective therapeutic methods for prevention and treatment other than valve replacement surgery.
This review summarizes the cellular and molecular mechanisms of calcific aortic valve disease, emphasizing the need for new therapeutic approaches beyond valve replacement.
May support targeted medical therapies for calcific aortic valve disease; leaves open whether modulating initiation or progression phases improves outcomes.
The review provides current data on the pathogenesis of calcific aortic valve disease (CAVD) — a widespread disease with unfavorable prognosis. Currently, there are no effective therapeutic methods for the prevention and treatment of this pathology with the exception of valve replacement surgery. The role of genetic and hereditary factors in the occurrence of CAVD is considered, the leading pathogenetic mechanisms are described taking into account the stage of the disease. In particular, in the initiation phase of calcification, deposition of oxidized lipoproteins in the cusps and local inflammation plays the leading role. In the progression phase, active ectopic calcification dominates, similar to the process of bone formation. The study of the pathogenesis of CAVD seems appropriate taking into account the prospect of developing new effective therapeutic and prophylactic approaches.
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Щеглова et al. (2019) conducted a review in calcific aortic valve disease (CAVD). The pathogenesis of calcific aortic valve disease involves oxidized lipoprotein deposition and inflammation in the initiation phase, and active ectopic calcification in the progression phase.
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