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Overexpression of endothelial nitric oxide synthase accelerates atherosclerotic lesion formation in apoE-deficient mice
Nitric oxide (NO) derived from endothelial NO synthase (eNOS) is regarded as a protective factor against atherosclerosis. Therefore, augmentation of eNOS expression or NO production by pharmacological intervention is postulated to inhibit atherosclerosis. We crossed eNOS-overexpressing (eNOS-Tg) mic...
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| Autors principals: | , , , , , , , , , , , |
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| Format: | Artigo |
| Idioma: | Inglês |
| Publicat: |
American Society for Clinical Investigation
2002
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| Matèries: | |
| Accés en línia: | https://ncbi.nlm.nih.gov/pmc/articles/PMC151086/ https://ncbi.nlm.nih.gov/pubmed/12163452 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1172/JCI15215 |
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