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Association between sRAGE, esRAGE levels and vascular inflammation: Analysis with 18F-fluorodeoxyglucose positron emission tomography

Authors :
Nan Hee Kim
Sungeun Kim
Soon Young Hwang
Sae Jeong Yang
Dong Seop Choi
Ji A Seo
Kyung Mook Choi
Sin Gon Kim
Sei Hyun Baik
Hye Jin Yoo
Hae Yoon Choi
Tae Nyun Kim
Source :
Atherosclerosis. 220:402-406
Publication Year :
2012
Publisher :
Elsevier BV, 2012.

Abstract

Background The receptor for advanced glycation end-products (RAGE) and its diverse ligands play a pivotal role in the development of cardiovascular disease. Soluble forms of RAGE (sRAGE), including the splice variant endogenous secretory RAGE (esRAGE), may neutralize AGE-RAGE mediated vascular damage by acting as a decoy. 18 F-fluorodeoxyglucose positron emission tomography (FDG-PET) is a novel imaging technique for detecting vascular inflammation. Methods We examined vascular inflammation measured using FDG-PET in 41 type 2 diabetes patients and 41 healthy control subjects in the right carotid artery. Vascular 18 F-FDG uptake was measured as the blood-normalized standardized uptake value (SUV), known as the target-to-background ratio (TBR). In addition, their relationship with carotid intima-media thickness (CIMT), estimated GFR (eGFR), and other cardiovascular risk factors was evaluated. Results Both mean and maximum TBR values were significantly higher in patients with type 2 diabetes compared to healthy subjects. After adjusting for age and gender, sRAGE levels were significantly correlated with both mean and maximum TBR values, but not with CIMT values. Multiple linear regression analysis showed that maximum TBR values were independently associated with sRAGE levels in addition to HbA1c and eGFR. Conclusions Circulating sRAGE showed significant association with TBR values measured using FDG-PET, which reflect vascular inflammation.

Details

ISSN :
00219150
Volume :
220
Database :
OpenAIRE
Journal :
Atherosclerosis
Accession number :
edsair.doi.dedup.....4e3c18a4fdeaa139f3d5b89a05566214
Full Text :
https://doi.org/10.1016/j.atherosclerosis.2011.11.008