软骨细胞是维持软骨终板稳态的关键成分，其功能衰退及凋亡是椎间盘退变的根源。自噬是调控细胞代谢、存活及凋亡的关键途径，对维持终板软骨细胞功能及稳态尤为重要。既往认为ω-3/6脂肪酸主要参与调节体内炎症过程.本课题组研究发现ω-3/ω-6还可参与调节细胞自噬，ω-3脂肪酸可促进细胞自噬，维持其存活，而ω-6脂肪酸则与之相反，且mTORC1信号通路可能在此过程中发挥重要调控作用，但其具体分子机制尚不明确。课题组预实验发现：fat-1转基因小鼠可将椎间盘终板软骨中omega-6转变成omega-3,为研究其作用及机制提供了重要基础。因此，本课题在前期研究工作基础上，旨在动物和分子水平，进一步深入研究omega-3/6脂肪酸调控终板软骨细胞mTORC1信号通路活性的机制，并探讨其直接和（或）间接调控终板软骨细胞自噬、存活及功能的分子机制。为明确椎间盘退变的发病机制及其防治策略提供新理论和新靶点。

Endplate chondrocyte play a key role in maitaining the homastasis of cartilage endplate. Loss of function and apoptosis of endplate cartilage chondrocyte are considered as the root of disc degeneration. Autophagy is a critical pathway that regulates cell metabolism, survival and apoptosis, which is particularly important maintaining of cartilage endplate homeostasis. Previous studies commonly suggested ω-3 and ω-6 faty acid involve in the regulation of inflammatory processes in vivo. Our team has found that ω-3 / ω-6 could involve in the regulation of autophagy. In our previous study, we found that: increasing ω-3 fatty acid content and reducing ω-6 fatty acid content, can promote cartilage autophagy to maintain its survival, and delay osteoarthritis in fat-1 transgenic mice model. Besides mTOR singaling pathway probably involving these activity, but the mechanism is unclear. Our preliminary experiments found: there were significantly increased ω-3 fatty acid and decreased ω-6 fatty acid in the intervertebral disc, which suggest ω-3 / ω-6 fatty acids in endplate cartilage may be involved in disc degeneration. This study intends to further study the role and mechanism of ω-3 and ω-6 fatty acids involving in endplate chondrocyte autophagy via mTORC1 singaling pathway, which could provide new perspective in the awareness and prevention of endplate cartilage degeneration.