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- W99202504 abstract "Neovascularization is important physiological repair mechanism in response to ischemic injury and its process is dependent on reactive oxygen species (ROS). Overproduction of superoxide anion (O2· −) rather contributes to various cardiovascular diseases. The extracellular superoxide dismutase (ecSOD) is the major antioxidant enzymes against O2· − in vascular extracellular space; however, its role in neovascularization induced by tissue ischemia is unknown. Here we show that hindlimb ischemia of mice stimulates a significant increase in ecSOD activity in ischemic tissues where ecSOD protein is highly expressed at arterioles. In mice lacking ecSOD, ischemia-induced increase in blood flow recovery, collateral vessel formation and capillary density are significantly inhibited as compared to wild-type (WT) mice (37.6 %, 36.5%, and 26.4% decrease, respectively). Impaired neovascularization in ecSOD knockout (KO) mice is associated with enhanced ischemia induced O2· − production by 1.5 fold, TUNEL-positive apopt..." @default.
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- W99202504 date "2007-10-16" @default.
- W99202504 modified "2023-10-18" @default.
- W99202504 title "Abstract 346: Essential Role of Extracellular SOD in Reparative Neovascularization Induced by Hindlimb Ischemia" @default.
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