Thiol oxidative stress induced by metabolic disorders amplifies macrophage chemotactic responses and accelerates atherogenesis and kidney injury in LDL receptor-deficient mice.

@article{Qiao2009ThiolOS,
  title={Thiol oxidative stress induced by metabolic disorders amplifies macrophage chemotactic responses and accelerates atherogenesis and kidney injury in LDL receptor-deficient mice.},
  author={Mu Qiao and Qingwei Zhao and Chi Fung Lee and Lisa R. Tannock and Eric J. Smart and Richard G. LeBaron and Clyde F. Phelix and Yolanda Marie Rangel and Reto H Asmis},
  journal={Arteriosclerosis, thrombosis, and vascular biology},
  year={2009},
  volume={29 11},
  pages={
          1779-86
        }
}
BACKGROUND Strengthening the macrophage glutathione redox buffer reduces macrophage content and decreases the severity of atherosclerotic lesions in LDL receptor-deficient (LDLR(-/-)) mice, but the underlying mechanisms were not clear. This study examined the effect of metabolic stress on the thiol redox state, chemotactic activity in vivo, and the recruitment of macrophages into atherosclerotic lesions and kidneys of LDL-R(-/-) mice in response to mild, moderate, and severe metabolic stress… CONTINUE READING
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Increased expression of cytosolic and mitochondrial glutathione reductase in macrophages inhibits atherosclerotic lesion development in LDL receptor-deficient mice

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