左侧肾癌伴下腔静脉（IVC）癌栓患者的健侧肾脏功能损害是该类疾病面临的重要临床问题。临床工作发现其损害过程包括三个阶段：①IVC癌栓形成过程中的慢性淤血性损害；②术中肾动脉、肾静脉阻断所致急性缺血性和淤血性损害；③去除阻断后的缺血再灌注损害。本课题组前期成功构建了肾门段IVC梗阻动物模型，完整重现了上述三个损害过程，并针对三个损害过程分别取材，初步发现Wnt信号通路的异常激活在肾脏损害过程中可能发挥关键作用。以前期工作为基础，本课题拟通过低糖低氧细胞模型、氧糖剥夺再复氧细胞模型的体外实验和肾门段IVC梗阻动物模型的体内实验，阐明健侧肾脏的损害过程，研究Wnt信号通路的异常激活在肾脏损害及修复过程中对炎症、凋亡及氧化应激等的影响机制,为阐明健侧肾脏的三个损害过程和探寻肾脏保护方法提供理论依据。

The impairment of contralateral renal function in patients with left renal cell carcinoma and inferior vena cava (IVC) cancer thrombus is an important clinical problem. There are three stages in the process of renal function damage in clinical work：1. chronic congestive damage in the formation of IVC tumor thrombus；2. acute ischemic and congestive damage caused by renal artery and renal vein occlusion during operation；3. ischemia reperfusion injury after blocking removal. Our group successfully constructed the animal model of IVC obstruction in renal hilar segment in the previous work, and completely reproduced the three damage processes mentioned above, and samples were taken for three damage processes respectively, and found that the abnormal activation of Wnt signaling pathway may play a key role in the process of kidney damage. In this study, we intend to elucidate the damage process of contralateral kidney by hypoglycemic hypoxic cell model, oxygen-glucose deprivation-reoxygenation cell model in vitro and IVC obstruction in renal hilar segment model in vivo, and to study the mechanism of abnormal activation of Wnt signaling pathway on inflammation, apoptosis and oxidative stress during kidney damage and repair, and to provide theoretical basis for elucidating the three damage processes of the contralateral kidney and exploring the methods of kidney protection.