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Cited by 285

The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.

Receptor for Advanced Glycation End Products Mediates Inflammation and Enhanced Expression of Tissue Factor in Vasculature of Diabetic Apolipoprotein E–Null Mice

Open access
Kislinger, Thomas, Tanji, Nozomu, Wendt, Thoralf, Qu, Wu, Lu, Yan, Ferran, Luis J., Taguchi, Akihiko, Olson, Kim, Bucciarelli, Loredana, Goova, Mouza, Hofmann, Marion A., Cataldegirmen, Guellue, D’Agati, Vivette, Pischetsrieder, Monika, Stern, David M., Schmidt, Ann Marie·2001·Arteriosclerosis, Thrombosis, and Vascular Biology

Abstract

Abstract —Advanced glycation end products (AGEs) and their cell surface receptor, RAGE, have been implicated in the pathogenesis of diabetic complications. Here, we studied the role of RAGE and expression of its proinflammatory ligands, EN-RAGEs (S100/calgranulins), in inflammatory events mediating cellular activation in diabetic tissue. Apolipoprotein E–null mice were rendered diabetic with streptozotocin at 6 weeks of age. Compared with nondiabetic aortas and kidneys, diabetic aortas and kidneys displayed increased expression of RAGE, EN-RAGEs, and 2 key markers of vascular inflammation, vascular cell adhesion molecule (VCAM)-1 and tissue factor. Administration of soluble RAGE, the extracellular domain of the receptor, or vehicle to diabetic mice for 6 weeks suppressed levels of VCAM-1 and tissue factor in the aorta, in parallel with decreased expression of RAGE and EN-RAGEs. Diabetic kidney demonstrated increased numbers of EN-RAGE–expressing inflammatory cells infiltrating the glomerulus and enhanced mRNA for transforming growth factor-β, fibronectin, and α 1 (IV) collagen. In mice treated with soluble RAGE, the numbers of infiltrating inflammatory cells and mRNA levels for these glomerular cytokines and components of extracellular matrix were decreased. These data suggest that activation of RAGE primes cells targeted for perturbation in diabetic tissues by the induction of proinflammatory mediators.

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Metadata

Authors
Kislinger, T., Tanji, N., Wendt, T., Qu, W., Lu, Y., Ferran, L. J., Taguchi, A., Olson, K., Bucciarelli, L., Goova, M., Hofmann, M. A., Cataldegirmen, G., D’Agati, V., Pischetsrieder, M., Stern, D. M., & Schmidt, A. M.
Venue
Arteriosclerosis, Thrombosis, and Vascular Biology
Published
2001-06
Volume
21
Issue
6
Pages
905-910
ISSN
  • 1079-5642 (ISSN-L)
  • 1524-4636
OpenAlex
W2170646719
Cited by
285
References
6
FWCI
10.10
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Receptor for Advanced Glycation End Products Mediates Inflammation and Enhanced Expression of Tissue Factor in Vasculature of Diabetic Apolipoprotein E–Null Mice. https://app.cochat.ai/papers/10.1161/01.atv.21.6.905
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Kislinger, T., Tanji, N., Wendt, T., Qu, W., Lu, Y., Ferran, L. J., Taguchi, A., Olson, K., Bucciarelli, L., Goova, M., Hofmann, M. A., Cataldegirmen, G., D’Agati, V., Pischetsrieder, M., Stern, D. M., & Schmidt, A. M. (2001). Receptor for Advanced Glycation End Products Mediates Inflammation and Enhanced Expression of Tissue Factor in Vasculature of Diabetic Apolipoprotein E–Null Mice. Arteriosclerosis, Thrombosis, and Vascular Biology. https://doi.org/10.1161/01.atv.21.6.905

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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.