Aortic valve stenosis: an active atheroinflammatory process. Export

@article{citeulike:1759835, abstract = {PURPOSE OF REVIEW: To summarize the current understanding of the pathobiology of aortic valve stenosis and portray the major advances in this field. RECENT FINDINGS: Stenotic aortic valves are characterized by atherosclerosis-like 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-like activity 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 bone formation 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. SUMMARY: Recent 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 is eagerly awaited.}, address = {aWihuri Research Institute, Helsinki, Finland bDivision of Cardiology, Helsinki University Central Hospital, Helsinki, Finland.}, author = {Helske, S. and Kupari, M. and Lindstedt, K. A. and Kovanen, P. T.}, citeulike-article-id = {1759835}, citeulike-linkout-0 = {http://dx.doi.org/10.1097/MOL.0b013e3282a66099}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/17885417}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=17885417}, doi = {10.1097/MOL.0b013e3282a66099}, issn = {0957-9672}, journal = {Curr Opin Lipidol}, month = {October}, number = {5}, pages = {483--491}, posted-at = {2007-10-12 11:26:07}, priority = {2}, title = {Aortic valve stenosis: an active atheroinflammatory process.}, url = {http://dx.doi.org/10.1097/MOL.0b013e3282a66099}, volume = {18}, year = {2007} }

TY - JOUR ID - citeulike:1759835 L3 - citeulike-article-id:1759835 N2 - PURPOSE OF REVIEW: To summarize the current understanding of the pathobiology of aortic valve stenosis and portray the major advances in this field. RECENT FINDINGS: Stenotic aortic valves are characterized by atherosclerosis-like 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-like activity 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 bone formation 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. SUMMARY: Recent 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 is eagerly awaited. IS - 5 JF - Curr Opin Lipidol SN - 0957-9672 AD - aWihuri Research Institute, Helsinki, Finland bDivision of Cardiology, Helsinki University Central Hospital, Helsinki, Finland. EP - 491 TI - Aortic valve stenosis: an active atheroinflammatory process. VL - 18 SP - 483 AU - Helske, S AU - Kupari, M AU - Lindstedt, KA AU - Kovanen, PT PY - 2007/10// UR - http://dx.doi.org/10.1097/MOL.0b013e3282a66099 ER -