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Aortic valve stenosis: an active atheroinflammatory process
发表状态：
Current Opinion in Lipidology , 18:483–491
研究团队：
Satu Helskea, Markku Kuparib, Ken A. Lindstedta and Petri T. Kovanen
研究内容：
综述主动脉瓣狭窄的病理生物学研究现状，并对该领域的研究进展进行综述。
Abstract：
Purpose of reviewTo summarize the current understanding of the pathobiology of aortic valve stenosis and portray the major advances in this field.Recent findingsStenotic aortic valves are characterized by atherosclerosislike lesions, consisting of activated inflammatory cells,including T lymphocytes, macrophages, and mast cells, and of lipid deposits, calcific nodules, and bone tissue. Active mediators of calcification and cells with osteoblast-likeactivity are present in diseased valves. Extracellular matrix remodeling, including collagen synthesis and elastin degradation by matrix metalloproteinases and cathepsins, contributes to leaflet stiffening. In experimental animals, hypercholesterolemia induces calcification and boneformation in aortic valves, which can be inhibited by statin treatment. The potential of statins to retard progression of aortic valve stenosis has also been recognized in clinical studies; however, further prospective trials are needed.Angiotensin II-forming enzymes are upregulated in stenotic valves. Angiotensin II may participate in profibrotic progression of aortic valve stenosis and may serve as a possible therapeutic target.SummaryRecent findings regarding the interaction of inflammatory cells, lipids, mediators of calcification, and renin– angiotensin system in stenotic valves support the current opinion of aortic valve stenosis being an actively regulated disease, potentially amenable to targeted molecular therapy. Evidence from prospective clinical studies iseagerly awaited.
