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Published on: October 26, 2020
RAGE blockade stabilizes established atherosclerosis in diabetic apolipoprotein E-null mice.
Loredana G Bucciarelli1, Thoralf Wendt, Wu Qu
1Division of Surgical Science, College of Physicians & Surgeons, Department of Surgery, Columbia University, New York, NY 10032, USA.
Circulation
|November 27, 2002
Summary
Blockading the Receptor for Advanced Glycation End products (RAGE) significantly reduced atherosclerosis progression in established diabetic mouse models. This suggests RAGE blockade could be a new strategy for treating advanced vascular disease in diabetes.
Area of Science:
- Cardiovascular Research
- Diabetes Complications
- Vascular Biology
Background:
- Previous research indicated that blocking Receptor for Advanced Glycation End products (RAGE) could hinder early atherosclerosis in diabetic mice.
- Assessing RAGE blockade's impact on established vascular disease is crucial for clinical applications.
Purpose of the Study:
- To investigate the role of RAGE in the progression of atherosclerosis in established diabetic apolipoprotein E-null mice.
- To test the hypothesis that RAGE blockade can impact established atherosclerotic lesions.
Main Methods:
- Diabetic and control apoE-null mice were treated with soluble RAGE (sRAGE) or albumin from 14 to 20 weeks of age.
- Atherosclerotic lesion area and complexity were analyzed.
- Parameters of inflammation and cell activation were assessed.
Main Results:
- Albumin-treated diabetic mice showed increased atherosclerotic lesion area and complexity.
- sRAGE treatment significantly reduced lesion area and complexity in diabetic mice.
- sRAGE treatment also decreased inflammation and cell activation markers.
Conclusions:
- Receptor for Advanced Glycation End products (RAGE) plays a role in both the formation and progression of atherosclerotic lesions in diabetic mice.
- RAGE blockade presents a potential therapeutic strategy for stabilizing established atherosclerosis and associated vascular inflammation in diabetic patients.
