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Dragun, D., Müller, D.N., Brasen, J.H., Fritsche, L., Nieminen-Kelha, M., Dechend, R., Kintscher, U., Rudolph, B., Hoebeke, J., Eckert, D., Mazak, I., Plehm, R., Schonemann, C., Unger, T., Budde, K., Neumayer, H.H., Luft, F.C. and Wallukat, G. (2005) Angiotensin II Type 1-Receptor Activating Antibodies in Renal-Allograft Rejection. The New England Journal of Medicine, 352, 558-569.
https://doi.org/10.1056/NEJMoa035717

has been cited by the following article:

• TITLE: The Role of Angiotensin II Type 1 Receptor-Activating Antibodies in Vascular Inflammation

  AUTHORS: Yanxiang Sun, Yong Yuan, Li Feng, Yan Wang

  KEYWORDS: AT1 Receptors, Autoantibody, Inflammation, Atherosclerosis

  JOURNAL NAME: World Journal of Cardiovascular Diseases, Vol.10 No.4, April 26, 2020

  ABSTRACT: Background: Studies demonstrated the autoantiboies against angiotension II type 1 receptor (AT1-AAs) could induce vascular endothelial dysfunction. Our objective is to investigate the effect of AT1-AAs on atherosclerosis. Methods: AT1-AAs were purified from sera of patients with primary hypertension. Thirty-six New Zealand white rabbits were underwent balloon-induced abdominal aortic endothelial injury and fed an atherogenic diet for 6 weeks and were randomly divided into six groups with different drugs for 4 weeks. The levels of AT1-AAs, tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in different stage were detected by ELISA. The abdominal aortas of rabbits were stained with hematoxylin and eosin. The expression of matrix metalloproteinases-2 (MMP-2) in aortic tissue was detected by Western blotting. Results: The levels of TNF-α in the eighth week (0.17 ± 0.04, 0.34 ± 0.08) and in the tenth week (0.23 ± 0.04, 0.54 ± 0.11) were significantly higher than that at the beginning of test (0.04 ± 0.03, 0.08 ± 0.02) in the group of AT1-AAs with low-dose and high-dose (P Conclusion: The results showed that the AT1-AAs could aggravate the inflammatory reaction and the plaque formation.