z-logo
open-access-imgOpen Access
Vascular endothelial cell-derived endothelin-1 mediates vascular inflammation and neointima formation following blood flow cessation
Author(s) -
Dyah Wulan Anggrahini,
Noriaki Emoto,
Kazuhiko Nakayama,
Bambang Widyantoro,
Suko Adiarto,
Naoko Iwasa,
Hidemi aka,
Yoshiyuki Rikitake,
Yaz Y. Kisanuki,
Masashi Yanagisawa,
Ken–ichi Hirata
Publication year - 2009
Publication title -
cardiovascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.774
H-Index - 219
eISSN - 1755-3245
pISSN - 0008-6363
DOI - 10.1093/cvr/cvp026
Subject(s) - neointima , inflammation , vascular smooth muscle , vascular remodelling in the embryo , vasoprotective , endothelin 1 , endothelial stem cell , endothelium , vasoconstriction , endothelin receptor , vascular endothelial growth factor c , medicine , vascular endothelial growth factor b , immunology , receptor , biology , vascular endothelial growth factor a , vascular endothelial growth factor , restenosis , nitric oxide , in vitro , biochemistry , smooth muscle , stent , vegf receptors
Although endothelin-1 (ET-1) has been suggested to contribute to the pathogenesis of neointima formation and atherosclerosis, the individual roles of ET-1 derived from certain cell types in this disease remain unclear. In this study, we determined the role of vascular endothelial ET-1 on vascular inflammation and neointima formation using vascular endothelial ET-1-knockout [ET-1(f/f); Tie2-Cre (+)] mice.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here
Accelerating Research

Address

John Eccles House
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom