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10.15420/ecr.2015.10.2.108 http://scihub22266oqcxt.onion/10.15420/ecr.2015.10.2.108 C4888946!4888946!27274771     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27274771&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Eur+Cardiol 2015 ; 10 (2): 108-12 Nephropedia Template TP {{tp|p=27274771|t=2015. Calcific Aortic Valve Disease: Molecular Mechanisms and Therapeutic Approaches |pdf=|usr=}}{{27274771}} gab.com Text Calcific Aortic Valve Disease: Molecular Mechanisms and Therapeutic Approaches JO: Eur Cardiol http://www.kidney.de/pget.php?&tw=1&pmid=27274771 #FOAvip Calcification occurs in atherosclerotic vascular lesions and in the aortic valve. Calcific aortic valve disease (CAVD) is a slow, progressive disorder that ranges from mild valve thickening without obstruction of blood flow, termed aortic sclerosis, to severe calcification with impaired leaflet motion, termed aortic stenosis. In the past, this process was thought to be ?degenerative? because of time-dependent wear and tear of the leaflets, with passive calcium deposition. The presence of osteoblasts in atherosclerotic vascular lesions and in CAVD implies that calcification is an active, regulated process akin to atherosclerosis, with lipoprotein deposition and chronic inflammation. If calcification is active, via pro-osteogenic pathways, one might expect that development and progression of calcification could be inhibited. The overlap in the clinical factors associated with calcific valve disease and atherosclerosis provides further support for a shared disease mechanism. In our recent research we used an in vitro porcine valve interstitial cell model to study spontaneous calcification and potential promoters and inhibitors. Using this model, we found that denosumab, a human monoclonal antibody targeting the receptor activator of nuclear factor-?B ligand may, at a working concentration of 50 ?g/mL, inhibit induced calcium deposition to basal levels. Twit Text FOAVip Calcific Aortic Valve Disease: Molecular Mechanisms and Therapeutic Approaches ????Eur Cardiol http://www.kidney.de/pget.php?&tw=1&pmid=27274771 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27274771 #FOAvip English Wikipedia <ref>{{Cite pmid|27274771}}</ref> Calcific Aortic Valve Disease: Molecular Mechanisms and Therapeutic Approaches #MMPMID27274771 Lerman DA; Prasad S; Alotti N Eur Cardiol 2015[Dec]; 10 (2): 108-12 PMID27274771show ga Calcification occurs in atherosclerotic vascular lesions and in the aortic valve. Calcific aortic valve disease (CAVD) is a slow, progressive disorder that ranges from mild valve thickening without obstruction of blood flow, termed aortic sclerosis, to severe calcification with impaired leaflet motion, termed aortic stenosis. In the past, this process was thought to be ?degenerative? because of time-dependent wear and tear of the leaflets, with passive calcium deposition. The presence of osteoblasts in atherosclerotic vascular lesions and in CAVD implies that calcification is an active, regulated process akin to atherosclerosis, with lipoprotein deposition and chronic inflammation. If calcification is active, via pro-osteogenic pathways, one might expect that development and progression of calcification could be inhibited. The overlap in the clinical factors associated with calcific valve disease and atherosclerosis provides further support for a shared disease mechanism. In our recent research we used an in vitro porcine valve interstitial cell model to study spontaneous calcification and potential promoters and inhibitors. Using this model, we found that denosumab, a human monoclonal antibody targeting the receptor activator of nuclear factor-?B ligand may, at a working concentration of 50 ?g/mL, inhibit induced calcium deposition to basal levels. äCalcific Aortic Valve Disease: Molecular Mechanisms and Therapeutic Ap(epmc).pdf DeepDyve Pubget Overpricing