Dysfunctional HDL and atherosclerotic cardiovascular disease.
Identifieur interne : 002062 ( Main/Exploration ); précédent : 002061; suivant : 002063Dysfunctional HDL and atherosclerotic cardiovascular disease.
Auteurs : Robert S. Rosenson [États-Unis] ; H Bryan Brewer [États-Unis] ; Benjamin J. Ansell [États-Unis] ; Philip Barter [Australie] ; M John Chapman [France] ; Jay W. Heinecke [États-Unis] ; Anatol Kontush [France] ; Alan R. Tall [États-Unis] ; Nancy R. Webb [États-Unis]Source :
- Nature reviews. Cardiology [ 1759-5010 ] ; 2016.
Descripteurs français
- KwdFr :
- Apolipoprotéine A-I (génétique), Apolipoprotéine A-I (métabolisme), Athérosclérose (physiopathologie), Complications du diabète (métabolisme), Humains, Lipoprotéines HDL (génétique), Lipoprotéines HDL (métabolisme), Macrophages (métabolisme), Tabagisme (effets indésirables), Tabagisme (métabolisme), Transporteur-1 à cassette liant l'ATP (métabolisme), Transporteurs ABC (métabolisme).
- MESH :
- effets indésirables : Tabagisme.
- génétique : Apolipoprotéine A-I, Lipoprotéines HDL.
- métabolisme : Apolipoprotéine A-I, Complications du diabète, Lipoprotéines HDL, Macrophages, Tabagisme, Transporteur-1 à cassette liant l'ATP, Transporteurs ABC.
- physiopathologie : Athérosclérose.
- Humains.
English descriptors
- KwdEn :
- ATP Binding Cassette Transporter 1 (metabolism), ATP-Binding Cassette Transporters (metabolism), Apolipoprotein A-I (genetics), Apolipoprotein A-I (metabolism), Atherosclerosis (physiopathology), Diabetes Complications (metabolism), Humans, Lipoproteins, HDL (genetics), Lipoproteins, HDL (metabolism), Macrophages (metabolism), Smoking (adverse effects), Smoking (metabolism).
- MESH :
- chemical , genetics : Apolipoprotein A-I, Lipoproteins, HDL.
- chemical , metabolism : ATP Binding Cassette Transporter 1, Apolipoprotein A-I, Lipoproteins, HDL.
- adverse effects : Smoking.
- metabolism : ATP-Binding Cassette Transporters, Diabetes Complications, Macrophages, Smoking.
- physiopathology : Atherosclerosis.
- Humans.
Abstract
High-density lipoproteins (HDLs) protect against atherosclerosis by removing excess cholesterol from macrophages through the ATP-binding cassette transporter A1 (ABCA1) and ATP-binding cassette transporter G1 (ABCG1) pathways involved in reverse cholesterol transport. Factors that impair the availability of functional apolipoproteins or the activities of ABCA1 and ABCG1 could, therefore, strongly influence atherogenesis. HDL also inhibits lipid oxidation, restores endothelial function, exerts anti-inflammatory and antiapoptotic actions, and exerts anti-inflammatory actions in animal models. Such properties could contribute considerably to the capacity of HDL to inhibit atherosclerosis. Systemic and vascular inflammation has been proposed to convert HDL to a dysfunctional form that has impaired antiatherogenic effects. A loss of anti-inflammatory and antioxidative proteins, perhaps in combination with a gain of proinflammatory proteins, might be another important component in rendering HDL dysfunctional. The proinflammatory enzyme myeloperoxidase induces both oxidative modification and nitrosylation of specific residues on plasma and arterial apolipoprotein A-I to render HDL dysfunctional, which results in impaired ABCA1 macrophage transport, the activation of inflammatory pathways, and an increased risk of coronary artery disease. Understanding the features of dysfunctional HDL or apolipoprotein A-I in clinical practice might lead to new diagnostic and therapeutic approaches to atherosclerosis.
DOI: 10.1038/nrcardio.2015.124
PubMed: 26323267
Affiliations:
- Australie, France, États-Unis
- Californie, District de Columbia, Kentucky, Nouvelle-Galles du Sud, Washington (État), État de New York, Île-de-France
- New York, Paris, Seattle, Sydney
- Université Columbia, Université de Washington
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Le document en format XML
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Rosenson</name><affiliation wicri:level="2"><nlm:affiliation>Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, NY</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation></author><author><name sortKey="Brewer, H Bryan" sort="Brewer, H Bryan" uniqKey="Brewer H" first="H Bryan" last="Brewer">H Bryan Brewer</name><affiliation wicri:level="2"><nlm:affiliation>Cardiovascular Research Institute, MedStar Research Institute, Washington Hospital Center, Washington, DC, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Cardiovascular Research Institute, MedStar Research Institute, Washington Hospital Center, Washington, DC</wicri:regionArea><placeName><region type="state">District de Columbia</region></placeName></affiliation></author><author><name sortKey="Ansell, Benjamin J" sort="Ansell, Benjamin J" uniqKey="Ansell B" first="Benjamin J" last="Ansell">Benjamin J. 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Heinecke</name><affiliation wicri:level="4"><nlm:affiliation>Division of Metabolism, Endocrinology and Nutrition, University of Washington, Seattle, WA, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Metabolism, Endocrinology and Nutrition, University of Washington, Seattle, WA</wicri:regionArea><placeName><region type="state">Washington (État)</region><settlement type="city">Seattle</settlement></placeName><orgName type="university">Université de Washington</orgName></affiliation></author><author><name sortKey="Kontush, Anatol" sort="Kontush, Anatol" uniqKey="Kontush A" first="Anatol" last="Kontush">Anatol Kontush</name><affiliation wicri:level="3"><nlm:affiliation>INSERM-ICAN Research Unit 1166 of the National Institute for Health and Medical Research at Pitié-Salpétrière University Hospital, Paris, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>INSERM-ICAN Research Unit 1166 of the National Institute for Health and Medical Research at Pitié-Salpétrière University Hospital, Paris</wicri:regionArea><placeName><region type="region">Île-de-France</region><region type="old region">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author><author><name sortKey="Tall, Alan R" sort="Tall, Alan R" uniqKey="Tall A" first="Alan R" last="Tall">Alan R. Tall</name><affiliation wicri:level="4"><nlm:affiliation>Department of Medicine, Columbia University, New York, NY, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Medicine, Columbia University, New York, NY</wicri:regionArea><placeName><region type="state">État de New York</region><settlement type="city">New York</settlement></placeName><orgName type="university">Université Columbia</orgName></affiliation></author><author><name sortKey="Webb, Nancy R" sort="Webb, Nancy R" uniqKey="Webb N" first="Nancy R" last="Webb">Nancy R. Webb</name><affiliation wicri:level="2"><nlm:affiliation>Pharmacology &Nutritional Sciences and Saha Cardiovascular Research Center, University of Kentucky College of Medicine, Lexington, KY, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Pharmacology &Nutritional Sciences and Saha Cardiovascular Research Center, University of Kentucky College of Medicine, Lexington, KY</wicri:regionArea><placeName><region type="state">Kentucky</region></placeName></affiliation></author></analytic><series><title level="j">Nature reviews. Cardiology</title><idno type="eISSN">1759-5010</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>ATP Binding Cassette Transporter 1 (metabolism)</term><term>ATP-Binding Cassette Transporters (metabolism)</term><term>Apolipoprotein A-I (genetics)</term><term>Apolipoprotein A-I (metabolism)</term><term>Atherosclerosis (physiopathology)</term><term>Diabetes Complications (metabolism)</term><term>Humans</term><term>Lipoproteins, HDL (genetics)</term><term>Lipoproteins, HDL (metabolism)</term><term>Macrophages (metabolism)</term><term>Smoking (adverse effects)</term><term>Smoking (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Apolipoprotéine A-I (génétique)</term><term>Apolipoprotéine A-I (métabolisme)</term><term>Athérosclérose (physiopathologie)</term><term>Complications du diabète (métabolisme)</term><term>Humains</term><term>Lipoprotéines HDL (génétique)</term><term>Lipoprotéines HDL (métabolisme)</term><term>Macrophages (métabolisme)</term><term>Tabagisme (effets indésirables)</term><term>Tabagisme (métabolisme)</term><term>Transporteur-1 à cassette liant l'ATP (métabolisme)</term><term>Transporteurs ABC (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Apolipoprotein A-I</term><term>Lipoproteins, HDL</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>ATP Binding Cassette Transporter 1</term><term>Apolipoprotein A-I</term><term>Lipoproteins, HDL</term></keywords><keywords scheme="MESH" qualifier="adverse effects" xml:lang="en"><term>Smoking</term></keywords><keywords scheme="MESH" qualifier="effets indésirables" xml:lang="fr"><term>Tabagisme</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Apolipoprotéine A-I</term><term>Lipoprotéines HDL</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>ATP-Binding Cassette Transporters</term><term>Diabetes Complications</term><term>Macrophages</term><term>Smoking</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Apolipoprotéine A-I</term><term>Complications du diabète</term><term>Lipoprotéines HDL</term><term>Macrophages</term><term>Tabagisme</term><term>Transporteur-1 à cassette liant l'ATP</term><term>Transporteurs ABC</term></keywords><keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Athérosclérose</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Atherosclerosis</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Humains</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">High-density lipoproteins (HDLs) protect against atherosclerosis by removing excess cholesterol from macrophages through the ATP-binding cassette transporter A1 (ABCA1) and ATP-binding cassette transporter G1 (ABCG1) pathways involved in reverse cholesterol transport. Factors that impair the availability of functional apolipoproteins or the activities of ABCA1 and ABCG1 could, therefore, strongly influence atherogenesis. HDL also inhibits lipid oxidation, restores endothelial function, exerts anti-inflammatory and antiapoptotic actions, and exerts anti-inflammatory actions in animal models. Such properties could contribute considerably to the capacity of HDL to inhibit atherosclerosis. Systemic and vascular inflammation has been proposed to convert HDL to a dysfunctional form that has impaired antiatherogenic effects. A loss of anti-inflammatory and antioxidative proteins, perhaps in combination with a gain of proinflammatory proteins, might be another important component in rendering HDL dysfunctional. The proinflammatory enzyme myeloperoxidase induces both oxidative modification and nitrosylation of specific residues on plasma and arterial apolipoprotein A-I to render HDL dysfunctional, which results in impaired ABCA1 macrophage transport, the activation of inflammatory pathways, and an increased risk of coronary artery disease. Understanding the features of dysfunctional HDL or apolipoprotein A-I in clinical practice might lead to new diagnostic and therapeutic approaches to atherosclerosis.</div></front></TEI><affiliations><list><country><li>Australie</li><li>France</li><li>États-Unis</li></country><region><li>Californie</li><li>District de Columbia</li><li>Kentucky</li><li>Nouvelle-Galles du Sud</li><li>Washington (État)</li><li>État de New York</li><li>Île-de-France</li></region><settlement><li>New York</li><li>Paris</li><li>Seattle</li><li>Sydney</li></settlement><orgName><li>Université Columbia</li><li>Université de Washington</li></orgName></list><tree><country name="États-Unis"><region name="État de New York"><name sortKey="Rosenson, Robert S" sort="Rosenson, Robert S" uniqKey="Rosenson R" first="Robert S" last="Rosenson">Robert S. Rosenson</name></region><name sortKey="Ansell, Benjamin J" sort="Ansell, Benjamin J" uniqKey="Ansell B" first="Benjamin J" last="Ansell">Benjamin J. Ansell</name><name sortKey="Brewer, H Bryan" sort="Brewer, H Bryan" uniqKey="Brewer H" first="H Bryan" last="Brewer">H Bryan Brewer</name><name sortKey="Heinecke, Jay W" sort="Heinecke, Jay W" uniqKey="Heinecke J" first="Jay W" last="Heinecke">Jay W. Heinecke</name><name sortKey="Tall, Alan R" sort="Tall, Alan R" uniqKey="Tall A" first="Alan R" last="Tall">Alan R. Tall</name><name sortKey="Webb, Nancy R" sort="Webb, Nancy R" uniqKey="Webb N" first="Nancy R" last="Webb">Nancy R. Webb</name></country><country name="Australie"><region name="Nouvelle-Galles du Sud"><name sortKey="Barter, Philip" sort="Barter, Philip" uniqKey="Barter P" first="Philip" last="Barter">Philip Barter</name></region></country><country name="France"><region name="Île-de-France"><name sortKey="Chapman, M John" sort="Chapman, M John" uniqKey="Chapman M" first="M John" last="Chapman">M John Chapman</name></region><name sortKey="Kontush, Anatol" sort="Kontush, Anatol" uniqKey="Kontush A" first="Anatol" last="Kontush">Anatol Kontush</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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