AI Article Synopsis
- The AGE-RAGE system is increasingly recognized as playing a key role in diabetic vascular complications, and its interaction with the renin-angiotensin system (RAS) is not fully understood.
- Angiotensin II (Ang II) enhances RAGE expression in endothelial cells, leading to increased soluble RAGE (sRAGE) levels, an effect that can be blocked by the Ang II receptor antagonist telmisartan.
- The study suggests that serum sRAGE levels may indicate endothelial RAGE expression, highlighting a potential connection between the AGE-RAGE system and RAS in vascular health, particularly in patients with essential hypertension.
Article Abstract
There is a growing body of evidence that the advanced glycation end product (AGE)-their receptor (RAGE) system plays a central role in the pathogenesis of diabetic vascular complication. The renin-angiotensin system (RAS) contributes to the development and progression of diabetic angiopathy as well. However, the cross-talk between the AGE-RAGE system and the RAS is not fully understood. In this study, we examined the role of angiotensin II (Ang II) type 1 receptor system for RAGE expression in cultured endothelial cells (ECs) and in patients with essential hypertension. Ang II up-regulated RAGE mRNA levels of microvascular ECs and subsequently increased the soluble form of RAGE (sRAGE) expression in the medium of ECs, both of which were completely blocked by telmisartan, a commercially available Ang II type 1 receptor antagonist. Furthermore, telmisartan was found to decrease serum levels of sRAGE in patients with essential hypertension. These results demonstrate that sRAGE is released from the cell surface of Ang-II-exposed ECs. Our present study indicates that a cross-talk exists between the AGE-RAGE system and the RAS and suggests that serum levels of sRAGE may reflect endothelial RAGE expression.
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| http://dx.doi.org/10.1016/j.mvr.2005.10.002 | DOI Listing |
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