HDL-targeted therapies: progress, failures and future.
Identifieur interne : 003515 ( PubMed/Checkpoint ); précédent : 003514; suivant : 003516HDL-targeted therapies: progress, failures and future.
Auteurs : Bronwyn A. Kingwell [Australie] ; M John Chapman [France] ; Anatol Kontush [France] ; Norman E. Miller [Royaume-Uni]Source :
- Nature reviews. Drug discovery [ 1474-1784 ] ; 2014.
Descripteurs français
- KwdFr :
- Acide nicotinique (effets indésirables), Acide nicotinique (métabolisme), Acide nicotinique (usage thérapeutique), Animaux, Apolipoprotéine A-I (agonistes), Apolipoprotéine A-I (génétique), Apolipoprotéine A-I (métabolisme), Essais cliniques comme sujet, Humains, Hypolipémiants (effets indésirables), Hypolipémiants (métabolisme), Hypolipémiants (usage thérapeutique), Lipoprotéines HDL (agonistes), Lipoprotéines HDL (métabolisme), Lipoprotéines HDL (sang), Lipoprotéines HDL (usage thérapeutique), Maladies cardiovasculaires (), Maladies cardiovasculaires (métabolisme), Maladies cardiovasculaires (sang), Modèles biologiques, Médicaments en essais cliniques (effets indésirables), Médicaments en essais cliniques (métabolisme), Médicaments en essais cliniques (usage thérapeutique), Phosphatidylcholine-Sterol O-Acyltransferase (effets indésirables), Phosphatidylcholine-Sterol O-Acyltransferase (génétique), Phosphatidylcholine-Sterol O-Acyltransferase (métabolisme), Phosphatidylcholine-Sterol O-Acyltransferase (usage thérapeutique), Protéines de transfert des esters de cholestérol (antagonistes et inhibiteurs), Protéines de transfert des esters de cholestérol (métabolisme), Protéines recombinantes (effets indésirables), Protéines recombinantes (métabolisme), Protéines recombinantes (usage thérapeutique), Régulation positive (), Thérapie moléculaire ciblée (effets indésirables).
- MESH :
- agonistes : Apolipoprotéine A-I, Lipoprotéines HDL.
- antagonistes et inhibiteurs : Protéines de transfert des esters de cholestérol.
- effets indésirables : Acide nicotinique, Hypolipémiants, Médicaments en essais cliniques, Phosphatidylcholine-Sterol O-Acyltransferase, Protéines recombinantes, Thérapie moléculaire ciblée.
- génétique : Apolipoprotéine A-I, Phosphatidylcholine-Sterol O-Acyltransferase.
- métabolisme : Acide nicotinique, Apolipoprotéine A-I, Hypolipémiants, Lipoprotéines HDL, Maladies cardiovasculaires, Médicaments en essais cliniques, Phosphatidylcholine-Sterol O-Acyltransferase, Protéines de transfert des esters de cholestérol, Protéines recombinantes.
- sang : Lipoprotéines HDL, Maladies cardiovasculaires.
- usage thérapeutique : Acide nicotinique, Hypolipémiants, Lipoprotéines HDL, Médicaments en essais cliniques, Phosphatidylcholine-Sterol O-Acyltransferase, Protéines recombinantes.
- Animaux, Essais cliniques comme sujet, Humains, Maladies cardiovasculaires, Modèles biologiques, Régulation positive.
English descriptors
- KwdEn :
- Animals, Apolipoprotein A-I (agonists), Apolipoprotein A-I (genetics), Apolipoprotein A-I (metabolism), Cardiovascular Diseases (blood), Cardiovascular Diseases (metabolism), Cardiovascular Diseases (prevention & control), Cholesterol Ester Transfer Proteins (antagonists & inhibitors), Cholesterol Ester Transfer Proteins (metabolism), Clinical Trials as Topic, Drugs, Investigational (adverse effects), Drugs, Investigational (metabolism), Drugs, Investigational (therapeutic use), Humans, Hypolipidemic Agents (adverse effects), Hypolipidemic Agents (metabolism), Hypolipidemic Agents (therapeutic use), Lipoproteins, HDL (agonists), Lipoproteins, HDL (blood), Lipoproteins, HDL (metabolism), Lipoproteins, HDL (therapeutic use), Models, Biological, Molecular Targeted Therapy (adverse effects), Niacin (adverse effects), Niacin (metabolism), Niacin (therapeutic use), Phosphatidylcholine-Sterol O-Acyltransferase (adverse effects), Phosphatidylcholine-Sterol O-Acyltransferase (genetics), Phosphatidylcholine-Sterol O-Acyltransferase (metabolism), Phosphatidylcholine-Sterol O-Acyltransferase (therapeutic use), Recombinant Proteins (adverse effects), Recombinant Proteins (metabolism), Recombinant Proteins (therapeutic use), Up-Regulation (drug effects).
- MESH :
- chemical , adverse effects : Drugs, Investigational, Hypolipidemic Agents, Niacin, Phosphatidylcholine-Sterol O-Acyltransferase, Recombinant Proteins.
- chemical , agonists : Apolipoprotein A-I, Lipoproteins, HDL.
- chemical , antagonists & inhibitors : Cholesterol Ester Transfer Proteins.
- chemical , blood : Lipoproteins, HDL.
- chemical , genetics : Apolipoprotein A-I, Phosphatidylcholine-Sterol O-Acyltransferase.
- chemical , metabolism : Apolipoprotein A-I, Cholesterol Ester Transfer Proteins, Drugs, Investigational, Hypolipidemic Agents, Lipoproteins, HDL, Niacin, Phosphatidylcholine-Sterol O-Acyltransferase, Recombinant Proteins.
- adverse effects : Molecular Targeted Therapy.
- blood : Cardiovascular Diseases.
- drug effects : Up-Regulation.
- metabolism : Cardiovascular Diseases.
- prevention & control : Cardiovascular Diseases.
- chemical , therapeutic use : Drugs, Investigational, Hypolipidemic Agents, Lipoproteins, HDL, Niacin, Phosphatidylcholine-Sterol O-Acyltransferase, Recombinant Proteins.
- Animals, Clinical Trials as Topic, Humans, Models, Biological.
Abstract
Since the discovery in the 1970s that plasma levels of high-density lipoprotein cholesterol (HDL-C) are inversely associated with cardiovascular outcome, it has been postulated that HDL is anti-atherogenic and that increasing HDL-C levels is a promising therapeutic strategy. However, the recent failure of three orally active, HDL-C-raising agents has introduced considerable controversy, prompting the question of whether increasing the cholesterol cargo of HDL in a non-selective manner is an effective pharmacological approach for the translation of its atheroprotective and vasculoprotective activities. The interrelationships between HDL-C concentration, HDL particle number and levels of diverse HDL particle subpopulations of defined composition are complex, as are their relationships with reverse cholesterol transport and other anti-atherogenic functions. Such complexity highlights the incompleteness of our understanding of the biology of HDL particles. This article examines the HDL hypothesis in molecular and mechanistic terms, focusing on features that have been addressed, those that remain to be tested, and potential new targets for future pharmacological interventions.
DOI: 10.1038/nrd4279
PubMed: 24854407
Affiliations:
- Australie, France, Royaume-Uni
- Angleterre, Oxfordshire, Île-de-France
- Oxford, Paris
- Université Pierre-et-Marie-Curie, Université d'Oxford
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Links to Exploration step
pubmed:24854407Le document en format XML
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term>
<term>Apolipoprotein A-I (agonists)</term>
<term>Apolipoprotein A-I (genetics)</term>
<term>Apolipoprotein A-I (metabolism)</term>
<term>Cardiovascular Diseases (blood)</term>
<term>Cardiovascular Diseases (metabolism)</term>
<term>Cardiovascular Diseases (prevention & control)</term>
<term>Cholesterol Ester Transfer Proteins (antagonists & inhibitors)</term>
<term>Cholesterol Ester Transfer Proteins (metabolism)</term>
<term>Clinical Trials as Topic</term>
<term>Drugs, Investigational (adverse effects)</term>
<term>Drugs, Investigational (metabolism)</term>
<term>Drugs, Investigational (therapeutic use)</term>
<term>Humans</term>
<term>Hypolipidemic Agents (adverse effects)</term>
<term>Hypolipidemic Agents (metabolism)</term>
<term>Hypolipidemic Agents (therapeutic use)</term>
<term>Lipoproteins, HDL (agonists)</term>
<term>Lipoproteins, HDL (blood)</term>
<term>Lipoproteins, HDL (metabolism)</term>
<term>Lipoproteins, HDL (therapeutic use)</term>
<term>Models, Biological</term>
<term>Molecular Targeted Therapy (adverse effects)</term>
<term>Niacin (adverse effects)</term>
<term>Niacin (metabolism)</term>
<term>Niacin (therapeutic use)</term>
<term>Phosphatidylcholine-Sterol O-Acyltransferase (adverse effects)</term>
<term>Phosphatidylcholine-Sterol O-Acyltransferase (genetics)</term>
<term>Phosphatidylcholine-Sterol O-Acyltransferase (metabolism)</term>
<term>Phosphatidylcholine-Sterol O-Acyltransferase (therapeutic use)</term>
<term>Recombinant Proteins (adverse effects)</term>
<term>Recombinant Proteins (metabolism)</term>
<term>Recombinant Proteins (therapeutic use)</term>
<term>Up-Regulation (drug effects)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Acide nicotinique (effets indésirables)</term>
<term>Acide nicotinique (métabolisme)</term>
<term>Acide nicotinique (usage thérapeutique)</term>
<term>Animaux</term>
<term>Apolipoprotéine A-I (agonistes)</term>
<term>Apolipoprotéine A-I (génétique)</term>
<term>Apolipoprotéine A-I (métabolisme)</term>
<term>Essais cliniques comme sujet</term>
<term>Humains</term>
<term>Hypolipémiants (effets indésirables)</term>
<term>Hypolipémiants (métabolisme)</term>
<term>Hypolipémiants (usage thérapeutique)</term>
<term>Lipoprotéines HDL (agonistes)</term>
<term>Lipoprotéines HDL (métabolisme)</term>
<term>Lipoprotéines HDL (sang)</term>
<term>Lipoprotéines HDL (usage thérapeutique)</term>
<term>Maladies cardiovasculaires ()</term>
<term>Maladies cardiovasculaires (métabolisme)</term>
<term>Maladies cardiovasculaires (sang)</term>
<term>Modèles biologiques</term>
<term>Médicaments en essais cliniques (effets indésirables)</term>
<term>Médicaments en essais cliniques (métabolisme)</term>
<term>Médicaments en essais cliniques (usage thérapeutique)</term>
<term>Phosphatidylcholine-Sterol O-Acyltransferase (effets indésirables)</term>
<term>Phosphatidylcholine-Sterol O-Acyltransferase (génétique)</term>
<term>Phosphatidylcholine-Sterol O-Acyltransferase (métabolisme)</term>
<term>Phosphatidylcholine-Sterol O-Acyltransferase (usage thérapeutique)</term>
<term>Protéines de transfert des esters de cholestérol (antagonistes et inhibiteurs)</term>
<term>Protéines de transfert des esters de cholestérol (métabolisme)</term>
<term>Protéines recombinantes (effets indésirables)</term>
<term>Protéines recombinantes (métabolisme)</term>
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<term>Régulation positive ()</term>
<term>Thérapie moléculaire ciblée (effets indésirables)</term>
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<term>Hypolipidemic Agents</term>
<term>Niacin</term>
<term>Phosphatidylcholine-Sterol O-Acyltransferase</term>
<term>Recombinant Proteins</term>
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<keywords scheme="MESH" type="chemical" qualifier="agonists" xml:lang="en"><term>Apolipoprotein A-I</term>
<term>Lipoproteins, HDL</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Cholesterol Ester Transfer Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Lipoproteins, HDL</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Apolipoprotein A-I</term>
<term>Phosphatidylcholine-Sterol O-Acyltransferase</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Apolipoprotein A-I</term>
<term>Cholesterol Ester Transfer Proteins</term>
<term>Drugs, Investigational</term>
<term>Hypolipidemic Agents</term>
<term>Lipoproteins, HDL</term>
<term>Niacin</term>
<term>Phosphatidylcholine-Sterol O-Acyltransferase</term>
<term>Recombinant Proteins</term>
</keywords>
<keywords scheme="MESH" qualifier="adverse effects" xml:lang="en"><term>Molecular Targeted Therapy</term>
</keywords>
<keywords scheme="MESH" qualifier="agonistes" xml:lang="fr"><term>Apolipoprotéine A-I</term>
<term>Lipoprotéines HDL</term>
</keywords>
<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Protéines de transfert des esters de cholestérol</term>
</keywords>
<keywords scheme="MESH" qualifier="blood" xml:lang="en"><term>Cardiovascular Diseases</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Up-Regulation</term>
</keywords>
<keywords scheme="MESH" qualifier="effets indésirables" xml:lang="fr"><term>Acide nicotinique</term>
<term>Hypolipémiants</term>
<term>Médicaments en essais cliniques</term>
<term>Phosphatidylcholine-Sterol O-Acyltransferase</term>
<term>Protéines recombinantes</term>
<term>Thérapie moléculaire ciblée</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Apolipoprotéine A-I</term>
<term>Phosphatidylcholine-Sterol O-Acyltransferase</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Cardiovascular Diseases</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Acide nicotinique</term>
<term>Apolipoprotéine A-I</term>
<term>Hypolipémiants</term>
<term>Lipoprotéines HDL</term>
<term>Maladies cardiovasculaires</term>
<term>Médicaments en essais cliniques</term>
<term>Phosphatidylcholine-Sterol O-Acyltransferase</term>
<term>Protéines de transfert des esters de cholestérol</term>
<term>Protéines recombinantes</term>
</keywords>
<keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Cardiovascular Diseases</term>
</keywords>
<keywords scheme="MESH" qualifier="sang" xml:lang="fr"><term>Lipoprotéines HDL</term>
<term>Maladies cardiovasculaires</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Drugs, Investigational</term>
<term>Hypolipidemic Agents</term>
<term>Lipoproteins, HDL</term>
<term>Niacin</term>
<term>Phosphatidylcholine-Sterol O-Acyltransferase</term>
<term>Recombinant Proteins</term>
</keywords>
<keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Acide nicotinique</term>
<term>Hypolipémiants</term>
<term>Lipoprotéines HDL</term>
<term>Médicaments en essais cliniques</term>
<term>Phosphatidylcholine-Sterol O-Acyltransferase</term>
<term>Protéines recombinantes</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Clinical Trials as Topic</term>
<term>Humans</term>
<term>Models, Biological</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Essais cliniques comme sujet</term>
<term>Humains</term>
<term>Maladies cardiovasculaires</term>
<term>Modèles biologiques</term>
<term>Régulation positive</term>
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<front><div type="abstract" xml:lang="en">Since the discovery in the 1970s that plasma levels of high-density lipoprotein cholesterol (HDL-C) are inversely associated with cardiovascular outcome, it has been postulated that HDL is anti-atherogenic and that increasing HDL-C levels is a promising therapeutic strategy. However, the recent failure of three orally active, HDL-C-raising agents has introduced considerable controversy, prompting the question of whether increasing the cholesterol cargo of HDL in a non-selective manner is an effective pharmacological approach for the translation of its atheroprotective and vasculoprotective activities. The interrelationships between HDL-C concentration, HDL particle number and levels of diverse HDL particle subpopulations of defined composition are complex, as are their relationships with reverse cholesterol transport and other anti-atherogenic functions. Such complexity highlights the incompleteness of our understanding of the biology of HDL particles. This article examines the HDL hypothesis in molecular and mechanistic terms, focusing on features that have been addressed, those that remain to be tested, and potential new targets for future pharmacological interventions.</div>
</front>
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<Abstract><AbstractText>Since the discovery in the 1970s that plasma levels of high-density lipoprotein cholesterol (HDL-C) are inversely associated with cardiovascular outcome, it has been postulated that HDL is anti-atherogenic and that increasing HDL-C levels is a promising therapeutic strategy. However, the recent failure of three orally active, HDL-C-raising agents has introduced considerable controversy, prompting the question of whether increasing the cholesterol cargo of HDL in a non-selective manner is an effective pharmacological approach for the translation of its atheroprotective and vasculoprotective activities. The interrelationships between HDL-C concentration, HDL particle number and levels of diverse HDL particle subpopulations of defined composition are complex, as are their relationships with reverse cholesterol transport and other anti-atherogenic functions. Such complexity highlights the incompleteness of our understanding of the biology of HDL particles. This article examines the HDL hypothesis in molecular and mechanistic terms, focusing on features that have been addressed, those that remain to be tested, and potential new targets for future pharmacological interventions.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kingwell</LastName>
<ForeName>Bronwyn A</ForeName>
<Initials>BA</Initials>
<AffiliationInfo><Affiliation>Baker IDI Heart and Diabetes Institute, Melbourne, Victoria 3004, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chapman</LastName>
<ForeName>M John</ForeName>
<Initials>MJ</Initials>
<AffiliationInfo><Affiliation>INSERM UMRS-939, Dyslipidemia and Atherosclerosis Research Unit, Pitié-Salpetriere Hospital, Université Pierre et Marie Curie, Paris 6, France.</Affiliation>
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