期刊
NATURE MEDICINE
卷 9, 期 2, 页码 183-190出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nm817
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资金
- NHLBI NIH HHS [HL60234, R01 HL057854, HL53458, HL67040, HL58688, HL5785405] Funding Source: Medline
Carbon monoxide (CO), one of the products of heme oxygenase action on heme, prevents arteriosclerotic lesions that occur following aorta transplantation; pre-exposure to 250 parts per million of CO for 1 hour before injury suppresses stenosis after carotid balloon injury in rats as well as in mice. The protective effect of CO is associated with a profound inhibition of graft leukocyte infiltration/activation as well as with inhibition of smooth muscle cell proliferation. The anti-proliferative effect of CO in vitro requires the activation of guanylate cyclase, the generation of cGMP, the activation of p38 mitogen-activated protein kinases and the expression of the cell cycle inhibitor p21(Cip1). These findings demonstrate a protective role for CO in vascular injury and support its use as a therapeutic agent.
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