骨关节炎软骨基质降解的调控机制是目前国际研究热点，对指导临床治疗具有重要意义。我们的前期研究发现新的促进骨关节炎软骨退变基质降解的核心分子且能与基质金属蛋白酶ADAMTS相互作用的蛋白，即PBXIP1。本研究拟对PBXIP1在骨关节炎软骨基质降解中的功能和调控机制进行研究，通过利用基因芯片、RNA-seq和ChIP-seq等技术深入研究PBXIP1对ADAMTS的调控机制；利用PBXIP1基因敲除小鼠进行micro-CT、MRI和组织病理学检测PBXIP1在骨关节炎软骨基质降解中的生物学功能；利用临床标本确定PBXIP1和ADAMTS表达的相关性及其临床意义，为阐明骨关节炎软骨退变基质降解的机制提供新的思路和潜在靶点。

Research on the regulatory mechanism of articular cartilage matrix degradation in osteoarthritis, which will guide clinical therapy, has been of recent interest worldwide. Our previous study found that PBXIP, a novel molecule, could promote the matrix degradation of osteoarthritis cartilage and interact with ADAMTS. This study investigates the mechanism and function of PBXIP in osteoarthritic cartilage matrix degradation. Gene chip, RNA-seq and ChIP-seq analysis technology will be used to study the effect of PBXIP on the regulation of ADAMTS. Knockout mice will be examined by micro-CT, MRI and pathological analysis to determine the biological function of PBXIP in osteoarthritis. The clinical samples will be used to reveal the clinical significance and relationship between the expression of PBXIP and ADAMTS, which will provide new ideas and potential targets for elucidating the mechanism of articular cartilage degeneration and degradation in osteoarthritis.