Department of Experimental and Clinical Medicine, University Magna Graecia of Catanzaro, 88100 Catanzaro, Italy.
Department of Health Sciences, University Magna Graecia of Catanzaro, 88100 Catanzaro, Italy.
Int J Mol Sci. 2021 Jan 18;22(2):913. doi: 10.3390/ijms22020913.
Calcific Aortic Valve Disease (CAVD) is the most common valvular heart disease in developed countries and in the ageing population. It is strongly correlated to median age, affecting up to 13% of the population over the age of 65. Pathophysiological analysis indicates CAVD as a result of an active and degenerative disease, starting with sclerosis and chronic inflammation and then leaflet calcification, which ultimately can account for aortic stenosis. Although CAVD has been firstly recognized as a passive event mostly resulting from a degenerative aging process, much evidences suggests that calcification arises from different active processes, involving both aortic valve-resident cells (valve endothelial cells, valve interstitial cells, mesenchymal stem cells, innate immunity cells) and circulating cells (circulating mesenchymal cells, immunity cells). Moreover, a role for the cell-derived "matrix vesicles" and extracellular matrix (ECM) components has also been recognized. The aim of this work is to review the cellular and molecular alterations occurring in aortic valve during CAVD pathogenesis, focusing on the role of ECM in the natural course of the disease.
钙化性主动脉瓣疾病（CAVD）是发达国家和老龄化人口中最常见的瓣膜性心脏病。它与年龄中位数密切相关，影响多达 13%的 65 岁以上人群。病理生理学分析表明，CAVD 是一种活跃和退行性疾病的结果，从硬化和慢性炎症开始，然后是瓣叶钙化，最终可导致主动脉瓣狭窄。尽管 CAVD 最初被认为是一种主要由退行性衰老过程引起的被动事件，但大量证据表明，钙化是由不同的活跃过程引起的，涉及主动脉瓣固有细胞（瓣膜内皮细胞、瓣膜间质细胞、间充质干细胞、固有免疫细胞）和循环细胞（循环间充质细胞、免疫细胞）。此外，细胞衍生的“基质小泡”和细胞外基质（ECM）成分的作用也已得到认可。本研究旨在综述 CAVD 发病机制中主动脉瓣发生的细胞和分子改变，重点关注 ECM 在疾病自然病程中的作用。
