软骨终板渗透是椎间盘的主要营养途径（约占80%），软骨终板异常钙化导致的营养障碍和酸负荷增加是椎间盘退变的始动因素之一。我们预实验发现酸负荷可引起终板软骨细胞骨钙素（钙化指标）分泌增加，自噬可抑制骨钙素分泌。因此推测，自噬能抑制终板软骨细胞钙化。但酸负荷如何调控自噬的信号通路机制尚不明确。我们前期研究还发现质子感知受体OGR1在终板软骨细胞表达，受酸负荷调节，引起Ca2+内流，而Ca2+可调控细胞自噬。由此提出假说：酸负荷下OGR1介导Ca2+依赖的信号通路参与调控自噬，并对终板软骨钙化产生重要影响。为验证本假说，我们拟通过特异性激活和抑制自噬，观察自噬对终板软骨细胞钙化和代谢的影响；采用过表达和沉默OGR1，检测其对自噬的影响；检测相关基因和蛋白分析OGR1下游自噬信号通路及其在终板软骨细胞钙化中作用。本研究将揭示OGR1、自噬与软骨终板钙化的发生关系及机制，为防治椎间盘退变提供新思路。

The permeability of vertebral cartilage endplate (CEP) is the main way for the nutrition of intervertebral disc (IVD) (about 80%). The pathologic calcification of CEP, which induces the poor nutrition and the acid environment of IVD, is one of the initiating factors in IVD degeneration. In the previous study, we found that acidosis caused the increasing secretion of osteocalcin (an index for calcification) in endplate chondrocytes, while autophagy inhibited its secretion. So we speculate that autophagy can inhibit the pathologic calcification of endplate cartilage. However, it remains unclear about the signaling pathways of acidosis-induced autophagy. Our previous studies also found that proton-sensing receptors OGR1 was expressed in rat endplate chondrocytes, and was regulated by acidosis and caused Ca2+ inflowing to activate autophagy. Therefore, we raise a hypothesis based on the previous studies: OGR1 mediated Ca2+dependent signaling pathways may be involved in regulating the autophagy, and plays an important role in the endplate cartilage calcification. To verify this hypothesis, we plan to firstly use specific activation and inhibition of autophagy to observe its impact on the endplate cartilage calcification and metabolism, and then over-express and silent OGR1 to observe the its impact on autophagy, and finally detect the gene and protein expression to analyse the OGR1 downstream signaling pathways in autophagy and its role in the endplate cartilage calcification. This study will try to reveal the relationship among OGR1, autophagy and cartilage endplate calcification and explore its mechanism, and it will provide a new view for prevention and treatment of intervertebral disc degeneration.