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High Density Lipoprotein - Should we Raise it?


Landmesser, Ulf (2012). High Density Lipoprotein - Should we Raise it? Current Vascular Pharmacology, 10(6):718-719.

Abstract

Low high-density lipoprotein (HDL) cholesterol levels are associated with an increased risk of coronary artery disease and myocardial infarction. Experimental studies have identified several potential anti-atherogenic properties of HDL, including promotion of macrophage cholesterol efflux, endothelial nitric oxide stimulation, anti-inflammatory and anti-thrombotic effects. These observations have lead to the important question of whether raising of HDL can reduce cardiovacular risk. Notably, recent studies have suggested that vascular effects of HDL can be highly heterogenous and are altered in patients with coronary disease or diabetes, that has been referred to as "HDL dysfunction". Moreover, studies using gene-targeted mice have indicated that genetic modifications leading to a similar increase of HDL cholesterol levels can either reduce (i.e. apoA1 transgene overexpression) or accelerate (i.e. SR-B1 deficiency) atherosclerosis, depending on the molecular target. These findings therefore suggest that HDL cholesterol levels alone are likely not sufficient as a readout for the vascular effects of HDL-targeted therapeutic interventions, since both, the vascular effects of on-treatment HDL as well as the underlying molecular mechanism used to elevate HDL cholesterol levels may represent critical determinants of the overall vascular effects of therapeutic interventions raising HDL-cholesterol levels. In summary, low HDL cholesterol plasma levels remain associated with an increased cardiovascular risk. However, the above findings suggest that careful clinical trial programms are needed to determine, which HDL raising therapeutic interventions may indeed exert vasoprotective effects.

Abstract

Low high-density lipoprotein (HDL) cholesterol levels are associated with an increased risk of coronary artery disease and myocardial infarction. Experimental studies have identified several potential anti-atherogenic properties of HDL, including promotion of macrophage cholesterol efflux, endothelial nitric oxide stimulation, anti-inflammatory and anti-thrombotic effects. These observations have lead to the important question of whether raising of HDL can reduce cardiovacular risk. Notably, recent studies have suggested that vascular effects of HDL can be highly heterogenous and are altered in patients with coronary disease or diabetes, that has been referred to as "HDL dysfunction". Moreover, studies using gene-targeted mice have indicated that genetic modifications leading to a similar increase of HDL cholesterol levels can either reduce (i.e. apoA1 transgene overexpression) or accelerate (i.e. SR-B1 deficiency) atherosclerosis, depending on the molecular target. These findings therefore suggest that HDL cholesterol levels alone are likely not sufficient as a readout for the vascular effects of HDL-targeted therapeutic interventions, since both, the vascular effects of on-treatment HDL as well as the underlying molecular mechanism used to elevate HDL cholesterol levels may represent critical determinants of the overall vascular effects of therapeutic interventions raising HDL-cholesterol levels. In summary, low HDL cholesterol plasma levels remain associated with an increased cardiovascular risk. However, the above findings suggest that careful clinical trial programms are needed to determine, which HDL raising therapeutic interventions may indeed exert vasoprotective effects.

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Additional indexing

Item Type:Journal Article, refereed, further contribution
Communities & Collections:04 Faculty of Medicine > Institute of Physiology
07 Faculty of Science > Institute of Physiology

04 Faculty of Medicine > University Hospital Zurich > Clinic for Cardiology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Language:English
Date:2012
Deposited On:11 Jan 2013 09:24
Last Modified:05 Apr 2016 16:15
Publisher:Bentham Science Publishers
ISSN:1570-1611
Publisher DOI:https://doi.org/10.2174/157016112803520710
PubMed ID:23259564

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