Tranilast Suppresses Vascular Chymase Expression and Neointima Formation in Balloon-Injured Dog Carotid Artery
Author(s) -
Naotaka Shiota,
Hideki Okunishi,
Shinji Takai,
Imao Mikoshiba,
Hiroshi Sakonjo,
Nobuo Shibata,
Mizuo Miyazaki
Publication year - 1999
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/01.cir.99.8.1084
Subject(s) - medicine , neointima , tranilast , chymase , balloon , cardiology , carotid arteries , restenosis , stent , immunology , mast cell
Activation of vascular chymase plays a major role in myointimal hypertrophy after vascular injury by augmenting the production of angiotensin (ANG) II. Because chymase is synthesized mainly in mast cells, we assumed that the chymase-dependent ANG II formation could be downregulated by tranilast, a mast cell-stabilizing antiallergic agent. We have assessed inhibitory effects of tranilast on neointima formation after balloon injury in the carotid artery of dogs, which share a similar ANG II-forming chymase with humans, and further explored the pathophysiological significance of vascular chymase.
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