| pubmed-article:18547543 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18547543 | lifeskim:mentions | umls-concept:C0023821 | lld:lifeskim |
| pubmed-article:18547543 | lifeskim:mentions | umls-concept:C1705241 | lld:lifeskim |
| pubmed-article:18547543 | lifeskim:mentions | umls-concept:C0205170 | lld:lifeskim |
| pubmed-article:18547543 | lifeskim:mentions | umls-concept:C1705242 | lld:lifeskim |
| pubmed-article:18547543 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:18547543 | pubmed:dateCreated | 2008-8-4 | lld:pubmed |
| pubmed-article:18547543 | pubmed:abstractText | Since the very first report showing the regression of established atherosclerotic lesions by means of high-density lipoprotein cholesterol (HDL-C) plasma fraction, much information has been generated about the protective role of HDL-C in atherosclerosis. Nonetheless, this positive point of view about HDL has been nearly surpassed since modern informations concerning torcetrapib have appeared. Disappointment was palpable when its pivotal morbidity-and-mortality clinical trial, ILLUMINATE, was abruptly stopped due to excess mortality amongst the group randomized to receive torcetrapib. In this work we will try to put things in perspective. Lowering low-density lipoprotein cholesterol (LDL-C) levels with statins is a proven strategy for reducing the cardiovascular disease (CVD) risk. Despite the impressive benefits of statins, there remain a significant proportion of treated patients in which cardiovascular events are not prevented. Low HDL-C levels are an important independent risk factor for CVD. There is a need to develop suitable therapies to reduce this residual risk through HDL-C related mechanisms. Therefore, we will first review HDL-C pathways and we will subsequently state the new pharmacological approaches to HDL-C metabolism. | lld:pubmed |
| pubmed-article:18547543 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18547543 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18547543 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:18547543 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18547543 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18547543 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18547543 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18547543 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:18547543 | pubmed:issn | 1873-2968 | lld:pubmed |
| pubmed-article:18547543 | pubmed:author | pubmed-author:BadimonJuan... | lld:pubmed |
| pubmed-article:18547543 | pubmed:author | pubmed-author:Santos-Galleg... | lld:pubmed |
| pubmed-article:18547543 | pubmed:author | pubmed-author:IbanezBorjaB | lld:pubmed |
| pubmed-article:18547543 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:18547543 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:18547543 | pubmed:volume | 76 | lld:pubmed |
| pubmed-article:18547543 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18547543 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18547543 | pubmed:pagination | 443-52 | lld:pubmed |
| pubmed-article:18547543 | pubmed:dateRevised | 2009-5-21 | lld:pubmed |
| pubmed-article:18547543 | pubmed:meshHeading | pubmed-meshheading:18547543... | lld:pubmed |
| pubmed-article:18547543 | pubmed:meshHeading | pubmed-meshheading:18547543... | lld:pubmed |
| pubmed-article:18547543 | pubmed:meshHeading | pubmed-meshheading:18547543... | lld:pubmed |
| pubmed-article:18547543 | pubmed:meshHeading | pubmed-meshheading:18547543... | lld:pubmed |
| pubmed-article:18547543 | pubmed:meshHeading | pubmed-meshheading:18547543... | lld:pubmed |
| pubmed-article:18547543 | pubmed:meshHeading | pubmed-meshheading:18547543... | lld:pubmed |
| pubmed-article:18547543 | pubmed:meshHeading | pubmed-meshheading:18547543... | lld:pubmed |
| pubmed-article:18547543 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:18547543 | pubmed:articleTitle | HDL-cholesterol: is it really good? Differences between apoA-I and HDL. | lld:pubmed |
| pubmed-article:18547543 | pubmed:affiliation | Atherothrombosis Research Unit, The Zena and Michael A. Wiener Cardiovascular Institute, Mount Sinai School of Medicine, One Gustave L. Levy Place, Box 1030, New York, NY 10029, USA. | lld:pubmed |
| pubmed-article:18547543 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18547543 | pubmed:publicationType | Review | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:18547543 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:18547543 | lld:pubmed |
