急性肾损伤（AKI）是临床常见危重病症，已成为终末期肾脏疾病（ESRD）的重要病因。明确AKI修复过程能为改善预后提供科学依据。基于文献报道和本课题组前期工作，我们认为低氧诱导因子1α（HIF-1α）在AKI修复中具有重要作用。在体外实验中，我们首次发现HIF-1α可以调控分化抑制因子1(ID1)，ID1可下调钙粘蛋白E（E-cadherin)，具有促进肾小管上皮细胞（TEC）去分化作用，提示HIF-1α可能通过ID1介导TEC去分化。此外，HIF-1α是miR-27a的转录因子，而miR-27a的靶基因如EGFR对AKI修复具有重要作用，故HIF-1α也可通过miR-27a所涉及的信号通路调控AKI修复。因此，通过条件性基因敲除小鼠AKI模型及体外实验，阐明HIF-1α调控ID1和miR-27a的信号通路，对于明确AKI修复相关分子机制，提供新的临床干预靶点，具有重要科学价值和临床意义。

Acute kidney injury(AKI) is a common clinical critical disease, which has become an important cause of end stage renal disease(ESRD). Understanding the repair process of AKI could provide scientific proof for better prognosis. Based on literature reports and the preliminary works of our research group, we believe that hypoxia inducible factor 1α(HIF-1α) plays an important role in repair process of AKI. We found firstly that HIF-1α can regulate inhibitor of differentiation 1(ID1) in vitro experiments, and ID1 could down-regulate E-cadherin, promoting the dedifferentiation of renal tubular epithelial cell(TEC), showing that HIF-1α may mediate the dedifferentiation of TEC through ID1. Besides, HIF-1α is a transcription factor of miR-27a, while the target genes of miR-27a such as EGFR have important functions during AKI repairation, so HIF-1α may also regulate AKI repairation through signal pathways which are related to miR-27a. Therefore, clarifying the HIF-1α-ID1/miR-27a signal pathways by in vivo AKI model of conditional gene knockout mouse and in vitro experiments is crucial to definite AKI repairation related molecular mechanisms, and provide novel clinical targets for intervention, which has important scientific value and clinical significance.