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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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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