AK143693是正常肝组织和肝缺血再灌注损伤组织Kupffer细胞中差异表达的、功能未知的一条LncRNA。我们前期研究发现肝缺血再灌注组织Kupffer中AK143693表达降低，而miR-233的表达水平升高，TANK表达水平降低。通过生物信息学发现miR-233可能既靶向性结合AK143693，同时又靶向性结合TANK。进一步AK143693过表达实验发现可以显著上调TANK表达，同时miR-233水平降低，提示TANK可能为AK143693的调控靶标，且miR-233可能也参与调控。据此我们提出“AK143693可能作为竞争性内源RNA结合miR-233调控Kupffer细胞TANK表达介导肝缺血再灌注损伤”的假说，拟在本研究中进行验证，并探讨其作用机制。相关研究国内外未见报道，本研究将有助于探索AK143693的功能，为肝脏缺血再灌注损伤的防治提供新的干预靶向。

AK143693, an unclear function lncRNA, was specially down-regulated in liver Kupffer cells identified from differential lncRNA expression profile in normal liver and ischemia-reperfusion injury of mouse liver.Our previous study indicated that AK143693 was more down-regulated expressed in Kupffer cells from ischemia-reperfusion injury of mouse liver.Further bioinformatic analysis and experiment data indicated that AK143693 could regulate TANK through interactions with miR-223.qRT-PCR shows that expression level of miR-223 increased significantly，which was negatively related to AK143693 level，while TANK expression was markedly reduced; Further study found that miR-223 level reduced after overexpression of AK143693 in Kupffer cells,and TANK expression was increased. We propounded a hypothesis that act as ceRNA, AK143693 could mediate ischemia-reperfusion injury of mouse liver through regulate TANK in Kupffer cell by the interactions with miR-223.We will further investigate the bioinformatics characteristics of AK143693. Adopting overexpression strategies,luciferase reporter gene assay,RIP,Northern blotting,western blot, and qRT-PCR.We intend to explicit the effect of AK143693 on cellular level and animal model. Up to now, there is no report of AK143693 in ischemia-reperfusion injury of mouse liver. This study may provide a new target for the gene targeted therapeutics of ischemia-reperfusion injury of liver.