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CCR2-Mediated Antiinflammatory Effects of Endothelial Tetrahydrobiopterin Inhibit Vascular Injury-Induced Accelerated Atherosclerosis
Author(s) -
Ziad A. Ali,
Christina A. Bursill,
Gillian Douglas,
Eileen McNeill,
Marianna Papaspyridonos,
Amy L. Tatham,
Jennifer K. Bendall,
Asim M. Akhtar,
Nicholas J. C. King,
David R. Greaves,
Keith M. Chan
Publication year - 2008
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.107.753558
Subject(s) - medicine , tetrahydrobiopterin , endothelial dysfunction , pharmacology , nitric oxide , nitric oxide synthase
Vascular injury results in loss of endothelial nitric oxide (NO), production of reactive oxygen species (ROS), and the initiation of an inflammatory response. Both NO and ROS modulate inflammation through redox-sensitive pathways. Tetrahydrobiopterin (BH4) is an essential cofactor for endothelial nitric oxide synthase (eNOS) that regulates enzymatic synthesis of either nitric oxide or ROS. We hypothesized that endothelial BH4 is an important regulator of inflammation and vascular remodeling.

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