Amelioration of Acute Tubular Necrosis in Ischemic Acute Renal Failure was Impaired in Mice Lucking Hypoxia Inducible Factor-1α Gene

突变小鼠（HIF-1 kd）表现出持续升高的血尿素氮（BUN）水平在缺血再灌注后，与对照组小鼠相比。另一方面，通过Ki-67的表达评价的细胞增殖在对照小鼠中与来自早期阶段的突变小鼠相比增加。因此，在突变小鼠肾脏中，缺血性损伤引起的组织损伤延长，肾功能恢复延迟。我们将根据基因芯片分析的结果进一步探讨这一问题的机制。

The mutant mice(HIF-1 kd) showed a prolonged elevation of blood urea nitrogen (BUN) levels up after ischemia-reperfusion, compared to the control mice. On the other hand, the cell proliferation that was evaluated by expression of Ki-67 increased in the control mice, in comparison with the mutant mice from early phase. Thus, tissue damage by ischemic injury was prolonged and recovery of renal function was delayin the mutant mice kidney. We are going to pursue further mechanism about this problem according to results of microarray analysis.