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Article ; Online: HDL and cardiovascular disease: atherogenic and atheroprotective mechanisms.

Navab, Mohamad / Reddy, Srinivasa T / Van Lenten, Brian J / Fogelman, Alan M

2011 Volume 8, Issue 4, Page(s) 222–232

Abstract: The lipoprotein HDL has two important roles: first, it promotes reverse cholesterol transport, and second, it modulates inflammation. Epidemiological studies show that HDL-cholesterol levels are inversely correlated with the risk of cardiovascular events. ...

Abstract	The lipoprotein HDL has two important roles: first, it promotes reverse cholesterol transport, and second, it modulates inflammation. Epidemiological studies show that HDL-cholesterol levels are inversely correlated with the risk of cardiovascular events. However, many patients who experience a clinical event have normal, or even high, levels of HDL cholesterol. Measuring HDL-cholesterol levels provides information about the size of the HDL pool, but does not predict HDL composition or function. The main component of HDL, apolipoprotein A-I (apo A-I), is largely responsible for reverse cholesterol transport through the macrophage ATP-binding cassette transporter ABCA1. Apo A-I can be damaged by oxidative mechanisms, which render the protein less able to promote cholesterol efflux. HDL also contains a number of other proteins that are affected by the oxidative environment of the acute-phase response. Modification of the protein components of HDL can convert it from an anti-inflammatory to a proinflammatory particle. Small peptides that mimic some of the properties of apo A-I have been shown in preclinical models to improve HDL function and reduce atherosclerosis without altering HDL-cholesterol levels. Robust assays to evaluate the function of HDL are needed to supplement the measurement of HDL-cholesterol levels in the clinic.
MeSH term(s)	Apolipoprotein A-I/metabolism ; Cardiovascular Diseases/pathology ; Cholesterol, HDL/metabolism ; Cholesterol, HDL/physiology ; Cholesterol, LDL/metabolism ; Cholesterol, LDL/physiology ; Humans ; Inflammation/pathology ; Oxidative Stress ; Risk Assessment ; Risk Factors
Chemical Substances	Apolipoprotein A-I ; Cholesterol, HDL ; Cholesterol, LDL
Language	English
Publishing date	2011-02-08
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2490375-9
ISSN	1759-5010 ; 1759-5002
ISSN (online)	1759-5010
ISSN	1759-5002
DOI	10.1038/nrcardio.2010.222
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Article ; Online: HDL as a biomarker, potential therapeutic target, and therapy.

Navab, Mohamad / Anantharamaiah, G M / Reddy, Srinivasa T / Van Lenten, Brian J / Fogelman, Alan M

Diabetes

2009 Volume 58, Issue 12, Page(s) 2711–2717

MeSH term(s)	Acute-Phase Reaction/metabolism ; Animals ; Animals, Inbred Strains ; Apolipoprotein A-I/metabolism ; Biomarkers ; Cholesterol, HDL/blood ; Cholesterol, HDL/metabolism ; Cholesterol, LDL/metabolism ; Coronary Disease/metabolism ; Diabetes Mellitus/metabolism ; Hemoglobins/metabolism ; Humans ; Hyperlipoproteinemia Type II/metabolism ; Leprosy/metabolism ; Lipid Peroxidation ; Lupus Erythematosus, Systemic/metabolism ; Metabolic Syndrome/metabolism ; Mice ; Obesity/metabolism ; Oxidative Stress ; Predictive Value of Tests ; Rabbits ; Risk Assessment ; Risk Factors
Chemical Substances	Apolipoprotein A-I ; Biomarkers ; Cholesterol, HDL ; Cholesterol, LDL ; Hemoglobins
Language	English
Publishing date	2009-11-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/db09-0538
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Article: The role of dysfunctional HDL in atherosclerosis.

Navab, Mohamad / Reddy, Srinivasa T / Van Lenten, Brian J / Anantharamaiah, G M / Fogelman, Alan M

Journal of lipid research

2008 Volume 50 Suppl, Page(s) S145–9

Abstract: This review focuses on HDL function in modulating LDL oxidation and LDL-induced inflammation. Dysfunctional HDL has been identified in animal models and humans with chronic inflammatory diseases including atherosclerosis. The loss of antiinflammatory ... ...

Abstract	This review focuses on HDL function in modulating LDL oxidation and LDL-induced inflammation. Dysfunctional HDL has been identified in animal models and humans with chronic inflammatory diseases including atherosclerosis. The loss of antiinflammatory function correlated with a loss of function in reverse cholesterol transport. In animal models and perhaps in humans, dysfunctional HDL can be improved by apoA-I mimetic peptides that bind oxidized lipids with high affinity.
MeSH term(s)	Animals ; Apolipoprotein A-I/metabolism ; Atherosclerosis/metabolism ; Biomimetic Materials/pharmacology ; Cholesterol, HDL/metabolism ; Cholesterol, LDL/metabolism ; Humans ; Oxidation-Reduction/drug effects
Chemical Substances	Apolipoprotein A-I ; Cholesterol, HDL ; Cholesterol, LDL
Language	English
Publishing date	2008-10-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80154-9
ISSN	1539-7262 ; 0022-2275
ISSN (online)	1539-7262
ISSN	0022-2275
DOI	10.1194/jlr.R800036-JLR200
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Article: Proinflammatory high-density lipoprotein results from oxidized lipid mediators in the pathogenesis of both idiopathic and associated types of pulmonary arterial hypertension.

Ross, David J / Hough, Greg / Hama, Susan / Aboulhosn, Jamil / Belperio, John A / Saggar, Rajan / Van Lenten, Brian J / Ardehali, Abbas / Eghbali, Mansoureh / Reddy, Srinivasa / Fogelman, Alan M / Navab, Mohamad

Pulmonary circulation

2015 Volume 5, Issue 4, Page(s) 640–648

Abstract: Pulmonary arterial hypertension (PAH) is characterized by abnormal elaboration of vasoactive peptides, endothelial cell dysfunction, vascular remodeling, and inflammation, which collectively contribute to its pathogenesis. We investigated the potential ... ...

Abstract	Pulmonary arterial hypertension (PAH) is characterized by abnormal elaboration of vasoactive peptides, endothelial cell dysfunction, vascular remodeling, and inflammation, which collectively contribute to its pathogenesis. We investigated the potential for high-density lipoprotein (HDL) dysfunction (i.e., proinflammatory effects) and abnormal plasma eicosanoid levels to contribute to the pathobiology of PAH and assessed ex vivo the effect of treatment with apolipoprotein A-I mimetic peptide 4F on the observed HDL dysfunction. We determined the "inflammatory indices" HII and LII for HDL and low-density lipoprotein (LDL), respectively, in subjects with idiopathic PAH (IPAH) and associated PAH (APAH) by an in vitro monocyte chemotaxis assay. The 4F was added ex vivo, and repeat LII and HII values were obtained versus a sham treatment. We further determined eicosanoid levels in plasma and HDL fractions from patients with IPAH and APAH relative to controls. The LIIs were significantly higher for IPAH and APAH patients than for controls. Incubation of plasma with 4F before isolation of LDL and HDL significantly reduced the LII values, compared with sham-treated LDL, for IPAH and APAH. The increased LII values reflected increased states of LDL oxidation and thereby increased proinflammatory effects in both cohorts. The HIIs for both PAH cohorts reflected a "dysfunctional HDL phenotype," that is, proinflammatory HDL effects. In contrast to "normal HDL function," the determined HIIs were significantly increased for the IPAH and APAH cohorts. Ex vivo 4F treatment significantly improved the HDL function versus the sham treatment. Although there was a significant "salutary effect" of 4F treatment, this did not entirely normalize the HII. Significantly increased levels for both IPAH and APAH versus controls were evident for the eicosanoids 9-HODE, 13-HODE, 5-HETE, 12-HETE, and 15-HETE, while no statistical differences were evident for comparisons of IPAH and APAH for the determined plasma eicosanoid levels in the HDL fractions. Our study has further implicated the putative role of "oxidant stress" and inflammation in the pathobiology of PAH. Our data suggest the influences on the "dysfunctional HDL phenotype" of increased oxidized fatty acids, which are paradoxically proinflammatory. We speculate that therapies that target either the "inflammatory milieu" or the "dysfunctional HDL phenotype," such as apoA-I mimetic peptides, may be valuable avenues of further research in pulmonary vascular diseases.
Language	English
Publishing date	2015-12-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	2638089-4
ISSN	2045-8940 ; 2045-8932
ISSN (online)	2045-8940
ISSN	2045-8932
DOI	10.1086/683695
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Article ; Online: Isolevuglandin-type lipid aldehydes induce the inflammatory response of macrophages by modifying phosphatidylethanolamines and activating the receptor for advanced glycation endproducts.

Guo, Lilu / Chen, Zhongyi / Amarnath, Venkataraman / Yancey, Patricia G / Van Lenten, Brian J / Savage, Justin R / Fazio, Sergio / Linton, MacRae F / Davies, Sean S

Antioxidants & redox signaling

2015 Volume 22, Issue 18, Page(s) 1633–1645

Abstract: Aims: Increased lipid peroxidation occurs in many conditions associated with inflammation. Because lipid peroxidation produces lipid aldehydes that can induce inflammatory responses through unknown mechanisms, elucidating these mechanisms may lead to ... ...

Abstract	Aims: Increased lipid peroxidation occurs in many conditions associated with inflammation. Because lipid peroxidation produces lipid aldehydes that can induce inflammatory responses through unknown mechanisms, elucidating these mechanisms may lead to development of better treatments for inflammatory diseases. We recently demonstrated that exposure of cultured cells to lipid aldehydes such as isolevuglandins (IsoLG) results in the modification of phosphatidylethanolamine (PE). We therefore sought to determine (i) whether PE modification by isolevuglandins (IsoLG-PE) occurred in vivo, (ii) whether IsoLG-PE stimulated the inflammatory responses of macrophages, and (iii) the identity of receptors mediating the inflammatory effects of IsoLG-PE. Results: IsoLG-PE levels were elevated in plasma of patients with familial hypercholesterolemia and in the livers of mice fed a high-fat diet to induce obesity and hepatosteatosis. IsoLG-PE potently stimulated nuclear factor kappa B (NFκB) activation and expression of inflammatory cytokines in macrophages. The effects of IsoLG-PE were blocked by the soluble form of the receptor for advanced glycation endproducts (sRAGE) and by RAGE antagonists. Furthermore, macrophages derived from the bone marrow of Ager null mice failed to express inflammatory cytokines in response to IsoLG-PE to the same extent as macrophages from wild-type mice. Innovation: These studies are the first to identify IsoLG-PE as a mediator of macrophage activation and a specific receptor, RAGE, which mediates its biological effects. Conclusion: PE modification by IsoLG forms RAGE ligands that activate macrophages, so that the increased IsoLG-PE generated by high circulating cholesterol levels or high-fat diet may play a role in the inflammation associated with these conditions.
MeSH term(s)	Aldehydes/metabolism ; Animals ; Humans ; Inflammation/metabolism ; Lipids/chemistry ; Macrophages/metabolism ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; NF-kappa B/metabolism ; Phosphatidylethanolamines/chemistry ; Phosphatidylethanolamines/metabolism ; Prostaglandins E/chemistry ; Pyrrolidines/chemistry ; Receptor for Advanced Glycation End Products/antagonists & inhibitors ; Receptor for Advanced Glycation End Products/genetics ; Receptor for Advanced Glycation End Products/metabolism
Chemical Substances	Aldehydes ; Lipids ; NF-kappa B ; Phosphatidylethanolamines ; Prostaglandins E ; Pyrrolidines ; Receptor for Advanced Glycation End Products ; phosphatidylethanolamine (39382-08-6)
Language	English
Publishing date	2015-06-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1483836-9
ISSN	1557-7716 ; 1523-0864
ISSN (online)	1557-7716
ISSN	1523-0864
DOI	10.1089/ars.2014.6078
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Article ; Online: High-density lipoprotein and 4F peptide reduce systemic inflammation by modulating intestinal oxidized lipid metabolism: novel hypotheses and review of literature.

Navab, Mohamad / Reddy, Srinivasa T / Van Lenten, Brian J / Buga, Georgette M / Hough, Greg / Wagner, Alan C / Fogelman, Alan M

Arteriosclerosis, thrombosis, and vascular biology

2012 Volume 32, Issue 11, Page(s) 2553–2560

Abstract: Oxidized phospholipids are found in the vasculature of animal models of atherosclerosis, in human atherosclerotic lesions, and in other inflammatory diseases. Oxidized phospholipids cause vascular and nonvascular cells to initiate an inflammatory ... ...

Abstract	Oxidized phospholipids are found in the vasculature of animal models of atherosclerosis, in human atherosclerotic lesions, and in other inflammatory diseases. Oxidized phospholipids cause vascular and nonvascular cells to initiate an inflammatory reaction. Metabolites of arachidonic acid, such as 12-hydroxyeicosatetraenoic acid, can mimic some of the inflammatory properties of oxidized phospholipids. In vitro and in vivo normal high-density lipoprotein (HDL), normal apolipoprotein A-I, and apolipoprotein A-I mimetic peptides, each likely acting in a different manner, prevent the inflammatory reaction characteristic of atherosclerosis, and this is associated with decreased levels of oxidized lipids in tissues and cells. HDL from animal models of atherosclerosis or from humans with atherosclerosis or from humans or animals with other chronic inflammatory diseases does not prevent the inflammatory reaction characteristic of atherosclerosis and may even enhance the inflammatory reaction. In mice and perhaps humans, ≈30% of the steady-state plasma HDL-cholesterol pool is derived from the small intestine. The metabolism of phospholipids by gut bacteria has been recently implicated in atherosclerosis in both mice and humans. Studies with apolipoprotein A-I mimetic peptides suggest that the small intestine is a major tissue regulating systemic inflammation in mouse models of atherosclerosis and may be important for determining the functionality of HDL.
MeSH term(s)	Animals ; Anti-Inflammatory Agents/pharmacology ; Arachidonic Acid/metabolism ; Atherosclerosis/immunology ; Atherosclerosis/metabolism ; Atherosclerosis/pathology ; Atherosclerosis/prevention & control ; Blood Vessels/immunology ; Blood Vessels/metabolism ; Blood Vessels/pathology ; Humans ; Inflammation/immunology ; Inflammation/metabolism ; Inflammation/pathology ; Inflammation/prevention & control ; Intestine, Small/drug effects ; Intestine, Small/metabolism ; Lipoproteins, HDL/metabolism ; Lipoproteins, LDL/metabolism ; Oxidation-Reduction ; Peptides/pharmacology ; Phospholipids/metabolism
Chemical Substances	AP-4F peptide ; Anti-Inflammatory Agents ; Lipoproteins, HDL ; Lipoproteins, LDL ; Peptides ; Phospholipids ; oxidized low density lipoprotein ; Arachidonic Acid (27YG812J1I)
Keywords	covid19
Language	English
Publishing date	2012-10-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/ATVBAHA.112.300282
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Article ; Online: Apo A-1 mimetic peptides as atheroprotective agents in murine models.

Navab, Mohamad / Anantharamaiah, G M / Reddy, Srinivasa T / Van Lenten, Brian J / Fogelman, Alan M

Current drug targets

2008 Volume 9, Issue 3, Page(s) 204–209

Abstract: The mouse has proven to be an excellent model for testing apolipoprotein mimetic peptides as agents to treat a variety of vascular inflammatory conditions including atherosclerosis, cognitive dysfunction associated with arteriole inflammation, chronic ... ...

Abstract	The mouse has proven to be an excellent model for testing apolipoprotein mimetic peptides as agents to treat a variety of vascular inflammatory conditions including atherosclerosis, cognitive dysfunction associated with arteriole inflammation, chronic rejection of transplanted hearts, and scleroderma. The mechanism of action appears to relate to the ability of these peptides to preferentially bind pro-inflammatory oxidized lipids and is independent of the chirality of the peptides since peptides synthesized from either D- or L-amino acids appear to be equally effective.
MeSH term(s)	Animals ; Apolipoprotein A-I/metabolism ; Apolipoprotein A-I/therapeutic use ; Atherosclerosis/metabolism ; Atherosclerosis/prevention & control ; Biomimetic Materials/metabolism ; Biomimetic Materials/therapeutic use ; Disease Models, Animal ; Humans ; Mice ; Peptides/metabolism ; Peptides/therapeutic use ; Protein Binding/physiology
Chemical Substances	Apolipoprotein A-I ; Peptides
Language	English
Publishing date	2008-03-13
Publishing country	United Arab Emirates
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2064859-5
ISSN	1873-5592 ; 1389-4501
ISSN (online)	1873-5592
ISSN	1389-4501
DOI	10.2174/138945008783755584
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Article ; Online: Understanding changes in high density lipoproteins during the acute phase response.

Van Lenten, Brian J / Reddy, Srinivasa T / Navab, Mohamad / Fogelman, Alan M

Arteriosclerosis, thrombosis, and vascular biology

2006 Volume 26, Issue 8, Page(s) 1687–1688

MeSH term(s)	Acute-Phase Reaction/blood ; Animals ; Apolipoprotein A-I ; Apolipoproteins A/metabolism ; Aryldialkylphosphatase/metabolism ; Hepatocytes/metabolism ; Humans ; Inflammation/metabolism ; Lipoproteins, HDL/blood ; Serum Amyloid A Protein/metabolism
Chemical Substances	Apolipoprotein A-I ; Apolipoproteins A ; Lipoproteins, HDL ; Serum Amyloid A Protein ; Aryldialkylphosphatase (EC 3.1.8.1)
Language	English
Publishing date	2006-08
Publishing country	United States
Document type	Comment ; Editorial ; Review
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/01.ATV.0000232522.47018.a6
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Article ; Online: L-4F differentially alters plasma levels of oxidized fatty acids resulting in more anti-inflammatory HDL in mice.

Imaizumi, Satoshi / Grijalva, Victor / Navab, Mohamad / Van Lenten, Brian J / Wagner, Alan C / Anantharamiah, G M / Fogelman, Alan M / Reddy, Srinivasa T

Drug metabolism letters

2010 Volume 4, Issue 3, Page(s) 139–148

Abstract: To determine in vivo if L-4F differentially alters plasma levels of oxidized fatty acids resulting in more anti-inflammatory HDL. Injecting L-4F into apoE null mice resulted in a significant reduction in plasma levels of 15-HETE, 5-HETE, 13-HODE and 9- ... ...

Abstract	To determine in vivo if L-4F differentially alters plasma levels of oxidized fatty acids resulting in more anti-inflammatory HDL. Injecting L-4F into apoE null mice resulted in a significant reduction in plasma levels of 15-HETE, 5-HETE, 13-HODE and 9-HODE. In contrast, plasma levels of 20-HETE were not reduced and plasma levels of 14,15-EET, which are derived from the cytochrome P450 pathway, were elevated after injection of L-4F. Injection of 13(S)-HPODE into wild-type C57BL/6J mice caused an increase in plasma levels of 13-HODE and 9-HODE and was accompanied by a significant loss in the anti-inflammatory properties of HDL. The response of atherosclerosis resistant C3H/HeJ mice to injection of 13(S)-HPODE was similar but much more blunted. Injection of L-4F at a site different from that at which the 13(S)-HPODE was injected resulted in significantly lower plasma levels of 13-HODE and 9-HODE and significantly less loss of HDL anti-inflammatory properties in both strains. i) L-4F differentially alters plasma levels of oxidized fatty acids in vivo. ii) The resistance of the C3H/HeJ strain to atherosclerosis may in part be mediated by a reduced reaction of this strain to these potent lipid oxidants.
MeSH term(s)	8,11,14-Eicosatrienoic Acid/analogs & derivatives ; 8,11,14-Eicosatrienoic Acid/blood ; Animals ; Anti-Inflammatory Agents/administration & dosage ; Apolipoproteins E/deficiency ; Apolipoproteins E/genetics ; Atherosclerosis/blood ; Atherosclerosis/genetics ; Atherosclerosis/prevention & control ; Chromatography, Liquid ; Enzyme-Linked Immunosorbent Assay ; Fatty Acids/blood ; Female ; Hydroxyeicosatetraenoic Acids/blood ; Injections, Subcutaneous ; Linoleic Acids/administration & dosage ; Linoleic Acids/blood ; Linoleic Acids, Conjugated/blood ; Lipid Peroxides/administration & dosage ; Lipoproteins, HDL/blood ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Knockout ; Oxidation-Reduction ; Peptides/administration & dosage ; Species Specificity ; Tandem Mass Spectrometry ; Time Factors ; Up-Regulation
Chemical Substances	Anti-Inflammatory Agents ; Apolipoproteins E ; Fatty Acids ; Hydroxyeicosatetraenoic Acids ; L-4F peptide ; Linoleic Acids ; Linoleic Acids, Conjugated ; Lipid Peroxides ; Lipoproteins, HDL ; Peptides ; 9-hydroxy-10,12-octadecadienoic acid (15514-85-9) ; 13-hydroperoxy-9,11-octadecadienoic acid (23017-93-8) ; 5-hydroxy-6,8,11,14-eicosatetraenoic acid (467RNW8T91) ; 13-hydroxy-9,11-octadecadienoic acid (5204-88-6) ; 15-hydroxy-5,8,11,13-eicosatetraenoic acid (73945-47-8) ; 14,15-epoxy-5,8,11-eicosatrienoic acid (81276-03-1) ; 8,11,14-Eicosatrienoic Acid (FC398RK06S)
Language	English
Publishing date	2010-08
Publishing country	United Arab Emirates
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1874-0758
ISSN (online)	1874-0758
DOI	10.2174/187231210791698438
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Article ; Online: Structure and function of HDL mimetics.

Navab, Mohamad / Shechter, Ishaiahu / Anantharamaiah, G M / Reddy, Srinivasa T / Van Lenten, Brian J / Fogelman, Alan M

Arteriosclerosis, thrombosis, and vascular biology

2009 Volume 30, Issue 2, Page(s) 164–168

Abstract: HDL mimetics have been constructed from a number of peptides and proteins with varying structures, all of which bind lipids found in HDL. HDL mimetics containing a peptide or protein have been constructed with as few as 4 and as many as 243 amino acid ... ...

Abstract	HDL mimetics have been constructed from a number of peptides and proteins with varying structures, all of which bind lipids found in HDL. HDL mimetics containing a peptide or protein have been constructed with as few as 4 and as many as 243 amino acid residues. Some HDL mimetics have been constructed with lipid but without a peptide or protein component. Some HDL mimetics promote cholesterol efflux, some have been shown to have a remarkable ability to bind oxidized lipids compared to human apolipoprotein A-I (apoA-I). Many of these peptides have been shown to have antiinflammatory properties. Based on studies in a number of animal models and in early human clinical trials, HDL mimetics appear to have promise as diagnostic and therapeutic agents.
MeSH term(s)	Administration, Oral ; Animals ; Anti-Inflammatory Agents/administration & dosage ; Anti-Inflammatory Agents/chemistry ; Anti-Inflammatory Agents/metabolism ; Anti-Inflammatory Agents/pharmacology ; Apolipoprotein A-I/metabolism ; Cardiovascular Diseases/drug therapy ; Cardiovascular Diseases/metabolism ; Cholesterol/metabolism ; Humans ; Hypolipidemic Agents/administration & dosage ; Hypolipidemic Agents/chemistry ; Hypolipidemic Agents/metabolism ; Hypolipidemic Agents/pharmacology ; Lipoproteins, HDL/chemistry ; Lipoproteins, HDL/metabolism ; Molecular Mimicry ; Oxidation-Reduction ; Peptides/administration & dosage ; Peptides/chemistry ; Peptides/metabolism ; Peptides/pharmacology ; Protein Binding ; Protein Conformation ; Structure-Activity Relationship
Chemical Substances	APOA1 protein, human ; Anti-Inflammatory Agents ; Apolipoprotein A-I ; Hypolipidemic Agents ; Lipoproteins, HDL ; Peptides ; Cholesterol (97C5T2UQ7J)
Language	English
Publishing date	2009-07-16
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/ATVBAHA.109.187518
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