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Cited by 337

The DOI matches its Crossref record; 33 of the 33 references it cites were found in a registry or an index.

Oxygenated Carotenoid Lutein and Progression of Early Atherosclerosis: The Los Angeles Atherosclerosis Study

Open access
Dwyer, James H., Navab, Mohamad, Dwyer, Kathleen M., Hassan, Kholood, Sun, Ping, Shircore, Anne, Hama-Levy, Susan, Hough, Greg, Wang, Xuping, Drake, Thomas, Merz, C. Noel Bairey, Fogelman, Alan M.·2001·Circulation
DOI 10.1161/01.cir.103.24.2922
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Abstract

Background —Carotenoids are hypothesized to explain some of the protective effects of fruit and vegetable intake on risk of cardiovascular disease. The present study assessed the protective effects of the oxygenated carotenoid lutein against early atherosclerosis. Methods and Results —Epidemiology: Progression of intima-media thickness (IMT) of the common carotid arteries over 18 months was determined ultrasonographically and was related to plasma lutein among a randomly sampled cohort of utility employees age 40 to 60 years (n=480). Coculture: The impact of lutein on monocyte response to artery wall cell modification of LDL was assessed in vitro by quantification of monocyte migration in a coculture model of human intima. Mouse models: The impact of lutein supplementation on atherosclerotic lesion formation was assessed in vivo by assigning apoE-null mice to chow or chow plus lutein (0.2% by weight) and LDL receptor–null mice to Western diet or Western diet plus lutein. IMT progression declined with increasing quintile of plasma lutein ( P for trend=0.007, age-adjusted; P =0.0007, multivariate). Covariate-adjusted IMT progression (mean±SEM) was 0.021±0.005 mm in the lowest quintile of plasma lutein, whereas progression was blocked in the highest quintile (0.004±0.005 mm; P =0.01). In the coculture, pretreatment of cells with lutein inhibited LDL-induced migration in a dose-dependent manner ( P <0.05). Finally, in the mouse models, lutein supplementation reduced lesion size 44% in apoE-null mice ( P =0.009) and 43% in LDL receptor–null mice ( P =0.02). Conclusions —These epidemiological, in vitro, and mouse model findings support the hypothesis that increased dietary intake of lutein is protective against the development of early atherosclerosis.

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Metadata

Authors
Dwyer, J. H., Navab, M., Dwyer, K. M., Hassan, K., Sun, P., Shircore, A., Hama-Levy, S., Hough, G., Wang, X., Drake, T., Merz, C. N. B., & Fogelman, A. M.
Venue
Circulation
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2001-06-19
Volume
103
Issue
24
Pages
2922-2927
ISSN
  • 0009-7322 (ISSN-L)
  • 1524-4539
DOI
10.1161/01.cir.103.24.2922
OpenAlex
W2035814904
Cited by
337
References
33
FWCI
8.91
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Oxygenated Carotenoid Lutein and Progression of Early Atherosclerosis: The Los Angeles Atherosclerosis Study. https://app.cochat.ai/papers/10.1161/01.cir.103.24.2922
The paper
Dwyer, J. H., Navab, M., Dwyer, K. M., Hassan, K., Sun, P., Shircore, A., Hama-Levy, S., Hough, G., Wang, X., Drake, T., Merz, C. N. B., & Fogelman, A. M. (2001). Oxygenated Carotenoid Lutein and Progression of Early Atherosclerosis: The Los Angeles Atherosclerosis Study. Circulation. https://doi.org/10.1161/01.cir.103.24.2922

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.