The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
Plasma Level of Endogenous Secretory RAGE Is Associated With Components of the Metabolic Syndrome and Atherosclerosis
Abstract
Objectives— Advanced glycation endproducts, AGEs, and its specific receptor, RAGE, are involved in diabetic vascular complications. Endogenous secretory RAGE, esRAGE, has been identified as an alternatively spliced form of RAGE, and shown to act as a decoy receptor for AGE. Here, we measured plasma esRAGE level with a recently developed enzyme-linked immunosorbent assay (ELISA) and examined its association with atherosclerosis in age- and gender-matched 203 type 2 diabetic and 134 nondiabetic subjects. Methods and Results— Plasma esRAGE was inversely associated with carotid or femoral atherosclerosis, as quantitatively measured as intimal-medial thickness (IMT) by arterial ultrasound. Stepwise regression analyses revealed that plasma esRAGE was the third strongest and independent factor associated with carotid IMT, following age and systolic blood pressure. Plasma esRAGE was significantly lower in diabetic patients (0.176±0.092 ng/mL) than nondiabetic controls (0.253±0.111). Of note, in all, diabetic or nondiabetic group, plasma esRAGE was significantly and inversely correlated with components of the metabolic syndrome including body mass index, blood pressure, triglyceride, HbA1c, or an insulin resistance index. Stepwise regression analyses showed that body mass index or insulin resistance index was the major factor determining plasma esRAGE in all, nondiabetic or diabetic population. Conclusions— esRAGE is a novel and potential protective factor for the metabolic syndrome and atherosclerosis.
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.
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
Atherosclerosis--an inflammatory disease
Ross, R. (1999) · New England Journal of Medicine · doi:10.1056/nejm199901143400207 · Cited by 21,725
Stratton, I. M. (2000) · BMJ · doi:10.1136/bmj.321.7258.405 · Cited by 9,059
Release of chromatin protein HMGB1 by necrotic cells triggers inflammation
Scaffidi, P., Misteli, T., & Bianchi, M. E. (2002) · Nature · doi:10.1038/nature00858 · Cited by 4,221
Danesh, J., Wheeler, J. G., Hirschfield, G. M., Eda, S., Eiriksdottir, G., Rumley, A., Lowe, G. D. O., Pepys, M. B., & Gudnason, V. (2004) · New England Journal of Medicine · doi:10.1056/nejmoa032804 · Cited by 2,953
New Criteria for `Obesity Disease' in Japan
The Examination Committee of Criter (2002) · Circulation Journal · doi:10.1253/circj.66.987 · Cited by 1,650
Tominaga, M., Eguchi, H., Manaka, H., Igarashi, K., Kato, T., & Sekikawa, A. (1999) · Diabetes Care · doi:10.2337/diacare.22.6.920 · Cited by 1,165
YONEKURA, H., YAMAMOTO, Y., SAKURAI, S., PETROVA, R. G., ABEDIN, M. J., LI, H., YASUI, K., TAKEUCHI, M., MAKITA, Z., TAKASAWA, S., et al. (2003) · Biochemical Journal · doi:10.1042/bj20021371 · Cited by 716
Self-citationEmoto, M., Nishizawa, Y., Maekawa, K., Hiura, Y., Kanda, H., Kawagishi, T., Shoji, T., Okuno, Y., & Morii, H. (1999) · Diabetes Care · doi:10.2337/diacare.22.5.818 · Cited by 457
Self-citationRage and arthritis: The G82S polymorphism amplifies the inflammatory response
Hofmann, M. A., Drury, S., Hudson, B. I., Gleason, M. R., Qu, W., Lu, Y., Lalla, E., Chitnis, S., Monteiro, J., Stickland, M. H., et al. (2002) · Genes & Immunity · doi:10.1038/sj.gene.6363861 · Cited by 383
Cited by
Perrone, A., Giovino, A., Benny, J., & Martinelli, F. (2020) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2020/3818196 · Cited by 459
Fishman, S. L., Sonmez, H., Basman, C., Singh, V., & Poretsky, L. (2018) · Molecular Medicine · doi:10.1186/s10020-018-0060-3 · Cited by 330
Maillard-Lefebvre, H., Boulanger, E., Daroux, M., Gaxatte, C., Hudson, B. I., & Lambert, M. (2009) · Rheumatology · doi:10.1093/rheumatology/kep199 · Cited by 190
Yamagishi, S.-I., Adachi, H., Nakamura, K., Matsui, T., Jinnouchi, Y., Takenaka, K., Takeuchi, M., Enomoto, M., Furuki, K., Hino, A., et al. (2006) · Metabolism · doi:10.1016/j.metabol.2006.05.007 · Cited by 148
Ueno, H., Koyama, H., Shoji, T., Monden, M., Fukumoto, S., Tanaka, S., Otsuka, Y., Mima, Y., Morioka, T., Mori, K., et al. (2010) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2010.04.006 · Cited by 65
Self-citationSaito, R., Araki, S., Yamamoto, Y., & Kusuhara, K. (2017) · Journal of Pediatric Endocrinology and Metabolism · doi:10.1515/jpem-2016-0262 · Cited by 8
Self-citation
Metadata
- Authors
- Koyama, H., Shoji, T., Yokoyama, H., Motoyama, K., Mori, K., Fukumoto, S., Emoto, M., Shoji, T., Tamei, H., Matsuki, H., Sakurai, S., Yamamoto, Y., Yonekura, H., Watanabe, T., Yamamoto, H., & Nishizawa, Y.
- Venue
- Arteriosclerosis, Thrombosis, and Vascular Biology
- Published
- 2005-12
- Volume
- 25
- Issue
- 12
- Pages
- 2587-2593
- ISSN
- 1079-5642 (ISSN-L)
- 1524-4636
- OpenAlex
- W2112132580
- Cited by
- 313
- References
- 9
- FWCI
- 13.21
- Type
- journal article
- Language
- en
- Open access
- closed
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
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.