The DOI matches its Crossref record; 99 of the 100 references it cites were found in a registry or an index.
Progress and challenges in translating the biology of atherosclerosis
Abstract
Atherosclerosis is a chronic disease of the arterial wall, and a leading cause of death and loss of productive life years worldwide. Research into the disease has led to many compelling hypotheses about the pathophysiology of atherosclerotic lesion formation and of complications such as myocardial infarction and stroke. Yet, despite these advances, we still lack definitive evidence to show that processes such as lipoprotein oxidation, inflammation and immunity have a crucial involvement in human atherosclerosis. Experimental atherosclerosis in animals furnishes an important research tool, but extrapolation to humans requires care. Understanding how to combine experimental and clinical science will provide further insight into atherosclerosis and could lead to new clinical applications.
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In the citing paper
“These symptoms are thought to further exacerbate inflammation and, in doing so, contribute to the pathogenesis of various diseases of aging (6–8), many of which involve excessive cytokine activity (9, 10).”
From Clustering of depression and inflammation in adolescents previously exposed to childhood adversity (2012) · cites this paper as [10]
In the citing paper
“Atherosclerosis originates from damaged endothelium that allows the accumulation of cholesterol-containing LDL particles in the arterial wall that tend to be oxidized, which triggers an inflammatory response that fails to resolve”
From Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty (2018) · cites this paper as [144]
In the citing paper
“These limitations are among the reasons that have motivated several groups to issue recommendations for accelerating the translation of nanoparticles into the clinic158,161,162.”
From Perspectives and opportunities for nanomedicine in the management of atherosclerosis (2011) · cites this paper as [162]
Citations
Cites
1 retracted
Toll-Like Receptor 2 Mediates Apolipoprotein CIII–Induced Monocyte Activation: Retracted
Kawakami, A., Osaka, M., Aikawa, M., Uematsu, S., Akira, S., Libby, P., Shimokado, K., Sacks, F. M., & Yoshida, M. (2008) · Circulation Research · doi:10.1161/circresaha.108.178426 · Cited by 76
Self-citationRetractedInflammation, Atherosclerosis, and Coronary Artery Disease
Hansson, G. K. (2005) · New England Journal of Medicine · doi:10.1056/nejmra043430 · Cited by 8,773
Self-citationEffects of Intensive Glucose Lowering in Type 2 Diabetes
(2008) · New England Journal of Medicine · doi:10.1056/nejmoa0802743 · Cited by 7,888
Rosuvastatin to Prevent Vascular Events in Men and Women with Elevated C-Reactive Protein
Ridker, P. M., Danielson, E., Fonseca, F. A. H., Genest, J., Gotto, A. M., Kastelein, J. J. P., Koenig, W., Libby, P., Lorenzatti, A. J., MacFadyen, J. G., et al. (2008) · New England Journal of Medicine · doi:10.1056/nejmoa0807646 · Cited by 6,674
Self-citationIntensive versus Moderate Lipid Lowering with Statins after Acute Coronary Syndromes
Cannon, C. P., Braunwald, E., McCabe, C. H., Rader, D. J., Rouleau, J. L., Belder, R., Joyal, S. V., Hill, K. A., Pfeffer, M. A., & Skene, A. M. (2004) · New England Journal of Medicine · doi:10.1056/nejmoa040583 · Cited by 4,938
Lusis, A. J. (2000) · Nature · doi:10.1038/35025203 · Cited by 4,880
Glucose control and vascular complications in veterans with type 2 diabetes
Duckworth, W., Abraira, C., Moritz, T., Reda, D., Emanuele, N., Reaven, P. D., Zieve, F. J., Marks, J., Davis, S. N., Hayward, R., et al. (2009) · New England Journal of Medicine · doi:10.1056/nejmoa0808431 · Cited by 4,762
NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals
Duewell, P., Kono, H., Rayner, K. J., Sirois, C. M., Vladimer, G., Bauernfeind, F. G., Abela, G. S., Franchi, L., Nuñez, G., Schnurr, M., et al. (2010) · Nature · doi:10.1038/nature08938 · Cited by 4,026
Helsinki Heart Study: Primary-Prevention Trial with Gemfibrozil in Middle-Aged Men with Dyslipidemia
Frick, M. H., Elo, O., Haapa, K., Heinonen, O. P., Heinsalmi, P., Helo, P., Huttunen, J. K., Kaitaniemi, P., Koskinen, P., Manninen, V., et al. (1987) · New England Journal of Medicine · doi:10.1056/nejm198711123172001 · Cited by 3,881 · cited 1×
“Clinical trials of one agent with PPAR-α-stimulating activity, gemfibrozil, have shown a reduction in cardiovascular event”
BackgroundRosuvastatin to Prevent Vascular Events in Men and Women With Elevated C-Reactive Protein
Ridker, P. M., Danielson, E., Fonseca, F. A. H., Genest, J. J., Gotto, A. M., Kastelein, J. J. P., Köenig, W., Libby, P., Lorenzatti, A. J., MacFadyen, J. G., et al. (2009) · Obstetrical & Gynecological Survey · doi:10.1097/01.ogx.0000344393.60303.0a · Cited by 3,641
Self-citation
Cited by
Sorted by citations
NF-κB signaling in inflammation
Liu, T., Zhang, L., Joo, D., & Sun, S.-C. (2017) · Signal Transduction and Targeted Therapy · doi:10.1038/sigtrans.2017.23 · Cited by 8,791
Macrophage biology in development, homeostasis and disease
Wynn, T. A., Chawla, A., & Pollard, J. W. (2013) · Nature · doi:10.1038/nature12034 · Cited by 4,684
Inflammation in Atherosclerosis
Libby, P. (2012) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.108.179705 · Cited by 3,796
Self-citationInflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty
Ferrucci, L., & Fabbri, E. (2018) · Nature Reviews Cardiology · doi:10.1038/s41569-018-0064-2 · Cited by 3,690
Endothelial Cell Dysfunction and the Pathobiology of Atherosclerosis
Gimbrone, M. A., & García‐Cardeña, G. (2016) · Circulation Research · doi:10.1161/circresaha.115.306301 · Cited by 3,694
Metadata
- Authors
- Libby, P., Ridker, P. M., & Hansson, G. K.
- Affiliations
- Brigham and Women's Hospital (US)
- Karolinska University Hospital (SE)
- Corresponding author
- Libby, Peter
- Venue
- Nature
- Published
- 2011-05
- Volume
- 473
- Issue
- 7347
- Pages
- 317-325
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W2033896075
- Semantic Scholar
- 31a83a618339a5f25357342f3633f5a423880eb6
- Cited by
- 4,010
- References
- 100
- Citations by year
- 2026: 169 · 2025: 235 · 2024: 252 · 2023: 249 · 2022: 283 · 2021: 342 · 2020: 299 · 2019: 264 · 2018: 271 · 2017: 304 · 2016: 271 · 2015: 286 · 2014: 258 · 2013: 232 · 2012: 230
- FWCI
- 22.29
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Keywords
- atherosclerosis, atherosclerotic plaque formation, lipoprotein oxidation, inflammation, immunity, animal models, animal-to-human extrapolation, myocardial infarction, stroke, translational research
- MeSH terms
- Animals, Humans, Inflammation, Cholesterol, HDL, Cholesterol, LDL, Triglycerides, Atherosclerosis, Lipid Metabolism
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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.
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