Cited by 150Cholesterol and Lipid MetabolismLipoproteins and Cardiovascular HealthParaoxonase enzyme and polymorphisms

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Novel HDL-directed pharmacotherapeutic strategies

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deGoma, Emil M., Rader, Daniel J.·2011·Nature Reviews Cardiology

DOI 10.1038/nrcardio.2010.200PMC PMC3315102

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Abstract

The burden of atherothrombotic cardiovascular disease remains high despite currently available optimum medical therapy. To address this substantial residual risk, the development of novel therapies that attempt to harness the atheroprotective functions of HDL is a major goal. These functions include the critical role of HDL in reverse cholesterol transport, and its anti-inflammatory, antithrombotic, and antioxidant activities. Discoveries in the past decade have shed light on the complex metabolic and antiatherosclerotic pathways of HDL. These insights have fueled the development of HDL-targeted drugs, which can be classified among four different therapeutic approaches: directly augmenting apolipoprotein A-I (apo A-I) levels, such as with apo A-I infusions and upregulators of endogenous apo A-I production; indirectly augmenting apo A-I and HDL-cholesterol levels, such as through inhibition of cholesteryl ester transfer protein or endothelial lipase, or through activation of the high-affinity niacin receptor GPR109A; mimicking the functionality of apo A-I with apo A-I mimetic peptides; and enhancing steps in the reverse cholesterol transport pathway, such as via activation of the liver X receptor or of lecithin-cholesterol acyltransferase.

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Anti-inflammatory apoA-I-mimetic peptides bind oxidized lipids with much higher affinity than human apoA-I
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Intestinal Specific LXR Activation Stimulates Reverse Cholesterol Transport and Protects from Atherosclerosis
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Compromised LCAT Function Is Associated With Increased Atherosclerosis
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Modulating cholesteryl ester transfer protein activity maintains efficient pre-β-HDL formation and increases reverse cholesterol transport
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Cholesteryl Ester Transfer Protein Taq I B2B2 Genotype Is Associated With Higher HDL Cholesterol Levels and Lower Risk of Coronary Heart Disease End Points in Men With HDL Deficiency
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Different roles of liver X receptor α and β in lipid metabolism: Effects of an α-selective and a dual agonist in mice deficient in each subtype
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D-4F and Statins Synergize to Render HDL Antiinflammatory in Mice and Monkeys and Cause Lesion Regression in Old Apolipoprotein E–Null Mice
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Liver X Receptor Activation Controls Intracellular Cholesterol Trafficking and Esterification in Human Macrophages
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Angiopoietin-like Protein 3 Mediates Hypertriglyceridemia Induced by the Liver X Receptor
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Tissue-Specific Liver X Receptor Activation Promotes Macrophage Reverse Cholesterol Transport In Vivo
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Large and Cholesteryl Ester-Rich High-Density Lipoproteins in Cholesteryl Ester Transfer Protein (CETP) Deficiency Can Not Protect Macrophages from Cholesterol Accumulation Induced by Acetylated Low-Density Lipoproteins1
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A new HDL mimetic peptide that stimulates cellular cholesterol efflux with high efficiency greatly reduces atherosclerosis in mice
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Increased Cholesterol Efflux Potential of Sera From ApoA-I Milano Carriers and Transgenic Mice
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Nicotinic Acid Receptor Agonists Differentially Activate Downstream Effectors
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The Liver X Receptor Ligand T0901317 Down-regulates APOA5 Gene Expression through Activation of SREBP-1c
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Dose-Related Effects of Repeated ETC-216 (Recombinant Apolipoprotein A-IMilano/1-Palmitoyl-2-Oleoyl Phosphatidylcholine Complexes) Administrations on Rabbit Lipid-Rich Soft Plaques
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Structural characterisation of the mouse nuclear oxysterol receptor genes LXRα and LXRβ
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Design of the DEFINE trial: Determining the EFficacy and Tolerability of CETP INhibition with AnacEtrapib
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Lecithin: Cholesterol Acyltransferase Expression Has Minimal Effects on Macrophage Reverse Cholesterol Transport In Vivo
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Endothelial lipase
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Apolipoprotein A-I mimetic peptides
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Structure/Function Relationships of Apolipoprotein A-I Mimetic Peptides
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High plasma cholesteryl ester transfer protein levels may favour reduced incidence of cardiovascular events in men with low triglycerides
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Gene transfer of wild-type apoA-I and apoA-I Milano reduce atherosclerosis to a similar extent
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The Pharmacology and Off-Target Effects of Some Cholesterol Ester Transfer Protein Inhibitors
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Production and Characterization of a Reconstituted High Density Lipoprotein for Therapeutic Applications
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Macrophage Reverse Cholesterol Transport in Mice Expressing ApoA-I Milano
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Bone Marrow Transplantation Shows Superior Atheroprotective Effects of Gene Therapy With Apolipoprotein A-I Milano Compared With Wild-Type Apolipoprotein A-I in Hyperlipidemic Mice
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Discovery of potent, selective sulfonylfuran urea endothelial lipase inhibitors
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Liver X Receptor and Farnesoid X Receptor as Therapeutic Targets
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Vaccinating Rabbits with a Cholesteryl Ester Transfer Protein (CETP) B-Cell Epitope Carried by Heat Shock Protein-65 (HSP65) for Inducing Anti-CETP Antibodies and Reducing Aortic Lesions In Vivo
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Wild-Type ApoA-I and the Milano Variant Have Similar Abilities to Stimulate Cellular Lipid Mobilization and Efflux
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Protective effect of an endothelial lipase gene variant on coronary artery disease in a Chinese population
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Authors: deGoma, E. M., & Rader, D. J.
Affiliations: University of Pennsylvania (US)
Corresponding author: deGoma, Emil M.
ORCID: deGoma, Emil M.
Rader, Daniel J.
Venue: Nature Reviews Cardiology
Publisher: Springer Science and Business Media LLC
Published: 2011-01-18
Volume: 8
Issue: 5
Pages: 266-277
ISSN: 1759-5002 (ISSN-L)
1759-5010
DOI: 10.1038/nrcardio.2010.200
PMC: PMC3315102
OpenAlex: W1984362422
Cited by: 149
References: 146
Citations by year: 2026: 1 · 2025: 2 · 2024: 5 · 2023: 4 · 2022: 2 · 2021: 4 · 2020: 4 · 2019: 6 · 2018: 6 · 2017: 7 · 2016: 11 · 2015: 10 · 2014: 13 · 2013: 29 · 2012: 29
FWCI: 5.09
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
www.springer.com/tdm (vor)
Locations: Nature Reviews Cardiology (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health (5k12hl083772-05, UL1TR000003)
National Heart, Lung, and Blood Institute (K12-HL083772, P50-HL70128, HL22633, K12 HL083772‑01, P01HL022633, P50HL070128)
National Center for Research Resources (UL1RR024134)
National Center for Advancing Translational Sciences
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Paraoxonase enzyme and polymorphisms
Keywords: apolipoprotein A-I, atherothrombotic cardiovascular disease, residual cardiovascular risk, reverse cholesterol transport, cholesteryl ester transfer protein inhibition, GPR109A, nicotinic acid, liver X receptor, lecithin:cholesterol acyltransferase, atheroprotection
MeSH terms: Animals, Hypolipidemic Agents, Cardiovascular Diseases, Humans, Cholesterol, HDL, Biomarkers, Apolipoprotein A-I, Treatment Outcome, Molecular Mimicry, Dyslipidemias, Lipid Metabolism

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