医学
细胞外基质
钙化
临床试验
临床实习
炎症
基础科学
生物信息学
主动脉瓣
狭窄
疾病
病理
重症监护医学
心脏病学
内科学
神经科学
细胞生物学
物理疗法
生物
作者
Kemal M. Akat,Martin Borggrefe,Jens J. Kaden
出处
期刊:Heart
[BMJ]
日期:2008-08-26
卷期号:95 (8): 616-623
被引量:89
标识
DOI:10.1136/hrt.2007.134783
摘要
Calcific aortic valve stenosis is the result of regulated cell processes. The histological hallmarks are inflammation and a remodelling of the extracellular matrix leading to bone formation. In the last 15 years the view has changed from it being an unmodifiable degenerative disease to an active biological process regulated by highly conserved ubiquitous cellular pathways. Many mechanisms and risk factors are the same as in atherosclerosis. Thus, statins and angiotensin II antagonists seemed promising treatment options. However, clinical trials failed to support this. This review describes the current understanding of major molecular mechanisms and discusses their role in clinical practice and possible therapy.
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