The DOI matches its Crossref record; 148 of the 148 references it cites were found in a registry or an index.
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.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“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]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Optimal Medical Therapy with or without PCI for Stable Coronary Disease
Boden, W. E., O'Rourke, R. A., Teo, K. K., Hartigan, P. M., Maron, D. J., Kostuk, W. J., Knudtson, M., Dada, M., Casperson, P., Harris, C. L., et al. (2007) · New England Journal of Medicine · doi:10.1056/nejmoa070829 · Cited by 4,699 · cited 1×
“In the best-case scenario of intensive treatment and vigilant monitoring, the incidence of 'hard' cardiovascular events in secondary prevention cohorts is 20% after 4–5 years”
BackgroundEffects of torcetrapib in patients at high risk for coronary events
Barter, P. J., Caulfield, M., Eriksson, M., Grundy, S. M., Kastelein, J. J. P., Komajda, M., Lopez-Sendon, J., Mosca, L., Tardif, J.-C., Waters, D. D., et al. (2007) · New England Journal of Medicine · doi:10.1056/nejmoa0706628 · Cited by 3,139
Nissen, S. E., Tuzcu, E. M., Schoenhagen, P., Brown, B. G., Ganz, P., Vogel, R. A., Crowe, T., Howard, G., Cooper, C. J., Brodie, B. R., et al. (2004) · JAMA · doi:10.1001/jama.291.9.1071 · Cited by 2,361
Brown, B. G., Zhao, X.-Q., Chait, A., Fisher, L. D., Cheung, M. C., Morse, J. S., Dowdy, A. A., Marino, E. K., Bolson, E. L., Alaupovic, P., et al. (2001) · New England Journal of Medicine · doi:10.1056/nejmoa011090 · Cited by 1,979
A Randomized Trial of Therapies for Type 2 Diabetes and Coronary Artery Disease
(2009) · New England Journal of Medicine · doi:10.1056/nejmoa0805796 · Cited by 1,939
Fifteen year mortality in Coronary Drug Project patients: long-term benefit with niacin
Canner, P. L., Berge, K. G., Wenger, N. K., Stamler, J., Friedman, L., Prineas, R. J., & Friedewald, W. (1986) · Journal of the American College of Cardiology · doi:10.1016/s0735-1097(86)80293-5 · Cited by 1,824
Repa, J. J., Liang, G., Ou, J., Bashmakov, Y. K., Lobaccaro, J. A., Shimomura, I., Shan, B., Brown, M. S., Goldstein, J. L., & Mangelsdorf, D. J. (2000) · Genes & Development · doi:10.1101/gad.844900 · Cited by 1,724
Nissen, S. E., Tsunoda, T., Tuzcu, E. M., Schoenhagen, P., Cooper, C. J., Yasin, M., Eaton, G. M., Lauer, M. A., Sheldon, W. S., Grines, C. L., et al. (2003) · JAMA · doi:10.1001/jama.290.17.2292 · Cited by 1,707
Peet, D. J., Turley, S. D., Ma, W., Janowski, B. A., Lobaccaro, J. A., Hammer, R. E., & Mangelsdorf, D. J. (1998) · Cell · doi:10.1016/s0092-8674(00)81432-4 · Cited by 1,466
Antiinflammatory Properties of HDL
Barter, P. J., Nicholls, S., Rye, K.-A., Anantharamaiah, G. M., Navab, M., & Fogelman, A. M. (2004) · Circulation Research · doi:10.1161/01.res.0000146094.59640.13 · Cited by 1,394
Cited by
Sorted by citations
HDL and cardiovascular disease
Rader, D. J., & Hovingh, G. K. (2014) · The Lancet · doi:10.1016/s0140-6736(14)61217-4 · Cited by 870
Self-citationInhibition of miR-33a/b in non-human primates raises plasma HDL and lowers VLDL triglycerides
Rayner, K. J., Esau, C. C., Hussain, F. N., McDaniel, A. L., Marshall, S. M., van Gils, J. M., Ray, T. D., Sheedy, F. J., Goedeke, L., Liu, X., et al. (2011) · Nature · doi:10.1038/nature10486 · Cited by 706
Molecular Biology of Atherosclerosis
Hopkins, P. N. (2013) · Physiological Reviews · doi:10.1152/physrev.00004.2012 · Cited by 469
Perspectives and opportunities for nanomedicine in the management of atherosclerosis
Lobatto, M. E., Fuster, V., Fayad, Z. A., & Mulder, W. J. M. (2011) · Nature Reviews Drug Discovery · doi:10.1038/nrd3578 · Cited by 423
Wang, H. H., Garruti, G., Liu, M., Portincasa, P., & Wang, D. Q. ‐. (2017) · Annals of Hepatology · doi:10.5604/01.3001.0010.5495 · Cited by 318
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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
