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Novel HDL-directed pharmacotherapeutic strategies
Open accessAbstract
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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“Among the various approaches of modulating HDL, direct infusions with recombinant HDL (rHDL) particles and augmenting APOA1 levels have been shown to be the most promising strategies54.”
From Perspectives and opportunities for nanomedicine in the management of atherosclerosis (2011) · cites this paper as [54]
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Metadata
- Authors
- deGoma, E. M., & Rader, D. J.
- Affiliations
- University of Pennsylvania (US)
- Corresponding author
- deGoma, Emil M.
- Venue
- Nature Reviews Cardiology
- Published
- 2011-01-18
- Volume
- 8
- Issue
- 5
- Pages
- 266-277
- ISSN
- 1759-5002 (ISSN-L)
- 1759-5010
- 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
- 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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