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Cited by 320

The DOI matches its Crossref record; 39 of the 39 references it cites were found in a registry or an index.

Troglitazone Inhibits Atherosclerosis in Apolipoprotein E–Knockout Mice: Pleiotropic Effects on CD36 Expression and HDL

Open access
Chen, Zhong, Ishibashi, Shun, Perrey, Stéphane, Osuga, Jun-ichi, Gotoda, Takanari, Kitamine, Tetsuya, Tamura, Yoshiaki, Okazaki, Hiroaki, Yahagi, Naoya, Iizuka, Yoko, Shionoiri, Futoshi, Ohashi, Ken, Harada, Kenji, Shimano, Hitoshi, Nagai, Ryozo, Yamada, Nobuhiro·2001·Arteriosclerosis, Thrombosis, and Vascular Biology

Abstract

Abstract —Atherosclerotic coronary heart disease is a common complication of the insulin resistance syndrome that can occur with or without diabetes mellitus. Thiazolidinediones (TZDs), which are insulin-sensitizing antidiabetic agents, can modulate the development of atherosclerosis not only by changing the systemic metabolic conditions associated with insulin resistance but also by exerting direct effects on vascular wall cells that express peroxisome proliferator–activated receptor-γ (PPAR-γ), a nuclear receptor for TZDs. Here we show that troglitazone, a TZD, significantly inhibited fatty streak lesion formation in apolipoprotein E–knockout mice fed a high-fat diet (en face aortic surface lesion areas were 6.9±2.5% vs 12.7±4.7%, P <0.05; cross-sectional lesion areas were 191 974±102 911 μm 2 vs 351 738±175 597 μm 2 , P <0.05; n=10). Troglitazone attenuated hyperinsulinemic hyperglycemia and increased high density lipoprotein cholesterol levels. In the aorta, troglitazone markedly increased the mRNA levels of CD36, a scavenger receptor for oxidized low density lipoprotein, presumably by upregulating its expression, at least in part, in the macrophage foam cells. These results indicate that troglitazone potently inhibits fatty streak lesion formation by modulating both metabolic extracellular environments and arterial wall cell functions.

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Crossref · 10.1161/01.atv.21.3.372

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Metadata

Authors
Chen, Z., Ishibashi, S., Perrey, S., Osuga, J.-I., Gotoda, T., Kitamine, T., Tamura, Y., Okazaki, H., Yahagi, N., Iizuka, Y., Shionoiri, F., Ohashi, K., Harada, K., Shimano, H., Nagai, R., & Yamada, N.
Venue
Arteriosclerosis, Thrombosis, and Vascular Biology
Published
2001-03
Volume
21
Issue
3
Pages
372-377
ISSN
  • 1079-5642 (ISSN-L)
  • 1524-4636
OpenAlex
W2086040049
Cited by
320
References
39
FWCI
12.81
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Troglitazone Inhibits Atherosclerosis in Apolipoprotein E–Knockout Mice: Pleiotropic Effects on CD36 Expression and HDL. https://app.cochat.ai/papers/10.1161/01.atv.21.3.372
The paper
Chen, Z., Ishibashi, S., Perrey, S., Osuga, J.-I., Gotoda, T., Kitamine, T., Tamura, Y., Okazaki, H., Yahagi, N., Iizuka, Y., Shionoiri, F., Ohashi, K., Harada, K., Shimano, H., Nagai, R., & Yamada, N. (2001). Troglitazone Inhibits Atherosclerosis in Apolipoprotein E–Knockout Mice: Pleiotropic Effects on CD36 Expression and HDL. Arteriosclerosis, Thrombosis, and Vascular Biology. https://doi.org/10.1161/01.atv.21.3.372

Data sources

Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

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.