Reperfusion of chronic tissue ischemia: nitrite and dipyridamole regulation of innate immune responses.
Reperfusion of chronic tissue ischemia: nitrite and dipyridamole regulation of innate immune responses.
复制标题
DOI:
10.1111/j.1749-6632.2010.05737.x
复制
发表时间:
2010-10
影响因子:
5.2
通讯作者:
Kevil CG
中科院分区:
文献类型:
--
作者:
Pattillo CB;Fang K;Terracciano J;Kevil CG
Chronic and intermittent ischemic vascular disorders represent a burgeoning clinical challenge. Previous studies have focused on the idea that therapeutic angiogenesis strategies could alleviate tissue ischemia; however, it is now appreciated that vascular disease is not simply limited to vascular wall cells but also influenced by simultaneously occurring inflammatory responses. Our laboratory has discovered that pharmacological treatment of permanent tissue ischemia with dipyridamole significantly augments ischemic tissue reperfusion, angiogenesis, and arteriogenesis over time. We have found that the beneficial effects of dipyridamole therapy are due to its ability to increase tissue nitric oxide bioavailability that corrects tissue redox imbalance. Importantly, we have also discovered that dipyridamole treatment invoking nitric oxide (NO) production significantly downregulates various innate immune response genes during chronic ischemic tissue injury. These findings demonstrate that dipyridamole induced production of nitrite/NO significantly decreases inflammatory responses while increasing vascular growth in ischemic tissues.
登录
查看更多内容
DOI:
10.1084/jem.190.10.1375
发表时间:
1999-11-15
期刊:
The Journal of experimental medicine
影响因子:
--
作者:
Hudson JD;Shoaibi MA;Maestro R;Carnero A;Hannon GJ;Beach DH
通讯作者:
Beach DH
DOI:
10.1016/j.bbrc.2006.10.010
发表时间:
2006-12-08
影响因子:
3.1
作者:
Ichikawa, Daiju;Funakoshi-Tago, Megumi;Kasahara, Tadashi
通讯作者:
Kasahara, Tadashi
影响因子:
3
作者:
Kusmic, C;Petersen, C;Barsacchi, R
通讯作者:
Barsacchi, R
影响因子:
4.4
作者:
Ruckdeschel, K;Mannel, O;Schröttner, P
通讯作者:
Schröttner, P
影响因子:
6.4
作者:
Garcia-Hernández, ML;Hernández-Pando, R;Berumen, J
通讯作者:
Berumen, J