尿石症是泌尿外科最常见的疾病之一，但是其发病机制目前仍不明确。经典的结石形成理论包括：尿液中晶体过饱和、晶体成核、晶体生长、晶体的聚集以及结晶的粘附，其中结晶的粘附是重要的致病因素。本课题组前期通过基因芯片筛选出lncRNA UCOO2KMD.1有促进晶体粘附的作用。根据生物信息学分析，我们发现UCOO2KMD.1与CD44有一段相同的碱基序列，且这段序列与miR-211-3p互补。研究表明，CD44和p38丝裂原活化蛋白激酶途径（MAPK）在晶体粘附过程中有重要的作用。由此，我们推测，UCOO2KMD.1通过竞争miR-211-3p参与CD44的调控，并参与激活p38 MAPK信号通路，从而影响晶体的粘附，最终导致结石形成。本项目拟通过研究UCOO2KMD.1、miR-211-3p、CD44和p38 MAPK信号通路在尿石形成中的作用及机制，为进一步阐明尿石症的发病机制提供依据。

Urolithiasis is one of the most common urological diseases; however, the pathogenesis is still unclear. Classical stone formation theories include: supersaturation of crystals in urine, nucleation of crystals, growth of crystals, aggregation of crystals and adhesion of crystals. Adhesion of crystals is an important pathogenic factor. In our previous study, lncRNA ucoo2kmd.1 was screened out to have the effect of promoting cell crystal adhesion through gene chip technology. According to the analysis of biological software, we found that ucoo2kmd.1 and CD44 have the same base sequence, and this base sequence is complementary to mir-211-3p. Previous studies have shown that CD44 and p38 mitogen-activated protein kinase (MAPK) pathways play an important role in cell adhesion. Therefore, we speculated that ucoo2kmd.1 participated in the regulation of CD44 by competing with mir-211-3p and regulating the p38 MAPK signaling pathway, thereby affecting the adhesion of crystals and ultimately leading to the formation of stones. This project aims to study the role and molecular mechanism of ucoo2kmd.1, mir-211-3p, CD44 and p38 MAPK signaling pathway in the process of renal stone formation, so as to further clarify the initial process of renal stone formation.