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10.1194/jlr.R026658 http://scihub22266oqcxt.onion/10.1194/jlr.R026658 22811413!3494258!22811413     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=22811413&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 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\22811413.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Lipid+Res 2012 ; 53 (12): 2515-24 Nephropedia Template TP {{tp|p=22811413|t=2012. The PCSK9 decade |pdf=|usr=}}{{22811413}} gab.com Text The PCSK9 decade JO: J Lipid Res http://www.kidney.de/pget.php?&tw=1&pmid=22811413 #FOAvip PCSK9 proprotein convertase subtilisin/kexin type (PCSK9) is a crucial protein in LDL cholesterol (LDL-C) metabolism by virtue of its pivotal role in the degradation of the LDL receptor. In recent years, both in vitro and in vivo studies have greatly supplemented our understanding of the (patho)physiological role of PCSK9 in human biology. In the current review, we summarize studies published or in print before May 2012 concerning the physiological role of PCSK9 in cholesterol metabolism. Moreover, we briefly describe the clinical phenotypes encountered in carriers of mutations in the gene encoding PCSK9. As PCSK9 has emerged as a novel target for LDL-C lowering therapy, methods to inhibit PCSK9 will also be reviewed. Initial data from investigations of PCSK9 inhibition in humans are promising and indicate that PCSK9 inhibition may be a viable new therapeutic option for the treatment of dyslipidemia and associated cardiovascular diseases. Twit Text FOAVip The PCSK9 decade ????J Lipid Res http://www.kidney.de/pget.php?&tw=1&pmid=22811413 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=22811413 #FOAvip English Wikipedia <ref>{{Cite pmid|22811413}}</ref> The PCSK9 decade #MMPMID22811413 Lambert G; Sjouke B; Choque B; Kastelein JJ; Hovingh GK J Lipid Res 2012[Dec]; 53 (12): 2515-24 PMID22811413show ga PCSK9 proprotein convertase subtilisin/kexin type (PCSK9) is a crucial protein in LDL cholesterol (LDL-C) metabolism by virtue of its pivotal role in the degradation of the LDL receptor. In recent years, both in vitro and in vivo studies have greatly supplemented our understanding of the (patho)physiological role of PCSK9 in human biology. In the current review, we summarize studies published or in print before May 2012 concerning the physiological role of PCSK9 in cholesterol metabolism. Moreover, we briefly describe the clinical phenotypes encountered in carriers of mutations in the gene encoding PCSK9. As PCSK9 has emerged as a novel target for LDL-C lowering therapy, methods to inhibit PCSK9 will also be reviewed. Initial data from investigations of PCSK9 inhibition in humans are promising and indicate that PCSK9 inhibition may be a viable new therapeutic option for the treatment of dyslipidemia and associated cardiovascular diseases. |*Proprotein Convertases/antagonists & inhibitors/genetics/metabolism[MESH] |*Serine Endopeptidases/genetics/metabolism[MESH] |Anticholesteremic Agents/pharmacology/therapeutic use[MESH] |Cardiovascular Diseases/drug therapy[MESH] |Cholesterol/metabolism[MESH] |Dyslipidemias/drug therapy[MESH] |Humans[MESH] |Hydroxymethylglutaryl-CoA Reductase Inhibitors/pharmacology/therapeutic use[MESH] |Phenotype[MESH]The PCSK9 decade (epmc).pdf DeepDyve Pubget Overpricing