我们前期的工作发现CTRP3可诱导血管平滑肌细胞（VSMC）向成骨表型转化并促进高磷诱导的VSMC钙化，但具体机制尚不明了。本项目以转录共激活因子PGC-1α为重点，线粒体生物生成和氧化应激为主线，采用线粒体呼吸测定、免疫荧光、基因敲低或过表达等方法在慢性肾衰大鼠、离体血管环和培养的VSMC观察单独CTRP3对线粒体生物生成和氧化应激的调节；CTRP3与高磷共同作用下线粒体生物生成和线粒体呼吸的变化及与VSMC表型转化和钙化的关系，明确PGC-1α是CTRP3调控VSMC线粒体生物生成、氧化应激以及VSMC表型转化和血管钙化的关键调控分子，并揭示CTRP3调控PGC-1α表达和活性的信号通路。我们的研究成果将有助于揭示CTRP3对线粒体生物生成和氧化应激的精细调控，加深对CTRP3促进血管钙化的分子机制的认识，也为临床防治血管钙化提供新的靶点与思路。

CTRP3 promotes vascular calcification by enhancing phosphate-induced osteogenic transition of VSMC. However, the exact mechanism involved is still unclear. Our study will focus on the effects of transcription coactivator PGC-1α, mitochondria biogenesis and reactive oxygen species (ROS) in CTRP3-promoted VSMC calcification. By using seahorse, immunofluorescence, gene knockdown and overexpression, we will explore the effects of CTRP3 on mitochondria biogenesis and oxidative stress in adenine-induced chronic renal failure rat, arterial ring calcification model and cultured VSMC. We will detect the effects of CTRP3 on mitochondria biogenesis, ROS production, phenotype switch and calcification of VSMC in the presence of βGP, aiming to determine that PGC-1α is the potential target for CTRP3-modulated mitochondria biogenesis, oxidative stress and VSMC calcification, and to clarify the signaling pathway involved in CTRP3-mediated expression and activity of PGC-1α. Our study will reveal the mechanism of CTRP3-mediated mitochondria biogenesis and oxidative stress, provide a new mechanism for CTRP3-promoted VSMC calcification and a potential target for therapeutic interference of vascular calcification.