强直性脊柱炎（ankylosing spondylitis，AS）脊柱关节强直畸形发生发展与机体成骨分化失调密切相关，研究强直性脊柱炎成骨分化调控机制对于指导临床意义重大。我们的前期研究发现SIX1与强直性脊柱炎成骨分化功能密切相关，并能与STAT3发生相互作用。在此基础上，本研究拟采用Western blot、实时免疫荧光定量PCR、ELISA测定SIX1在强直性脊柱炎成骨分化中的表达水平及变化趋势；采用μCT、组织病理学等对SIX1在体内外实验中的生物学功能进行检测；利用RNA-seq、ChIP-seq、基因芯片等对SIX1在强直性脊柱炎成骨分化中的分子调控机制进行探讨；通过临床标本分析确定SIX1和成骨分化调控因子的相关性及其临床意义，为研究强直性脊柱炎脊柱关节强直畸形的机制提供理论支持，并为确立强直性脊柱炎的诊断和治疗靶标提供新的思路。

The development of ankylosing spondylitis (AS) is closely related to the dysregulation of osteogenesis and differentiation of the body. Studying the regulation mechanism of osteogenic differentiation of AS is of great significance for guiding clinical practice. Our previous study showed that SIX1 is closely correlated with osteogenesis and differentiation function of AS and can interact with STAT3. Based on this, we will determine the expression of SIX1 in the osteogenesis and differentiation of AS by using Western blot, quantitative real-time PCR and ELISA assay. The biological function of SIX1 will be detected by using μCT and histopathology in vitro and in vivo experiments. The molecular regulatory mechanisms of SIX1 in osteogenesis and differentiation of AS will be investigated by using RNA-seq, ChIP-seq and gene chip assay. The correlation between SIX1 and osteogenic differentiation regulators and its clinical significance will be investigated by analysis of clinical specimens, which will provide theoretical support for the study of the mechanism of spinal deformity caused by AS, and new ideas for establishing the diagnostic and therapeutic targets for AS.