Overexpression of endothelial nitric oxide synthase accelerates atherosclerotic lesion formation in apoE-deficient mice.

@article{Ozaki2002OverexpressionOE,
  title={Overexpression of endothelial nitric oxide synthase accelerates atherosclerotic lesion formation in apoE-deficient mice.},
  author={M. Ozaki and S. Kawashima and T. Yamashita and T. Hirase and M. Namiki and N. Inoue and K. Hirata and H. Yasui and H. Sakurai and Y. Yoshida and M. Masada and M. Yokoyama},
  journal={The Journal of clinical investigation},
  year={2002},
  volume={110 3},
  pages={
          331-40
        }
}
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) mice with atherogenic apoE-deficient (apoE-KO) mice to determine whether eNOS overexpression in the endothelium could inhibit the development of atherosclerosis. After 8 weeks on a high-cholesterol diet… Expand
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  • Seinosuke Kawashima, T. Yamashita, +7 authors M. Yokoyama
  • Biology, Medicine
  • Arteriosclerosis, thrombosis, and vascular biology
  • 2001
Enhanced atherosclerosis and kidney dysfunction in eNOS(-/-)Apoe(-/-) mice are ameliorated by enalapril treatment.
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