细胞外基质（ECM）合成与降解失衡是椎间盘退变过程中重要的病理生理改变。非编码RNA作为重要的RNA分子，参与了细胞代谢的几乎所有病理生理过程，但是相关椎间盘退变的研究尚少。本研究基于对椎间盘标本中lncRNA、miRNA和mRNA的芯片数据分析及基因关联性分析，筛选出芯片中失调的ECM代谢失衡相关基因，并结合lncRNA和miRNA芯片分析、软件预测和预实验佐证结果，提出lncRNA TRPC7-AS1与COL1A2/HPN/CTSD竞争性结合miR-4769-5p，在椎间盘退变的过程中起重要作用的假说。本研究拟在人原代髓核细胞中和SD大鼠模型中进行进一步研究，深入探讨lncRNA TRPC7-AS1、miR-4769-5p和COL1A2/HPN/CTSD在椎间盘退变中的相互作用和影响机制，丰富和深化椎间盘退变发生发展的病理过程，以期为椎间盘退变的防治提供潜在靶点和新的思路。

The imbalance of extracellular matrix (ECM) synthesis and degradation is one of the most critical pathophysiological changes in the development of intervertebral disc degeneration (IDD). Non-coding RNAs are involved in almost all pathophysiological processes of cellular metabolism, but their roles and mechanisms in IDD are yet not clear. In the present study, based on lncRNA, miRNA and mRNA microarray analysis in IDD specimens, as well as the results of genetic correlation analysis, online tools predictions and pre-experiments, the genes related to dysregulation of ECM synthesis and degradation in IDD were screened and selected. To further investigation, we hypothesize that lncRNA TRPC7-AS1 may compete with COL1A2/HPN/CTSD for miR-4769-5p binding to modulate the process of IDD. This study attempts to investigate the interaction and molecular mechanism of lncRNA TRPC7-AS1, miR-4769-5p, and COL1A2/HPN/CTSD in human primary nucleus pulposus cells and in SD rat models, in order to reveal the pathological process and development of IDD, and to provide potential targets and novel theoretical basis for the prevention and treatment of IDD.