He Xianwei, Wu Liwei, Zhou Hao
Department of Orthopedic, Jinshan Hospital, Fudan University, Shanghai, China.
Heart Center and Shanghai Institute of Pediatric Congenital Heart Disease, Shanghai Children's Medical Center, National Children's Medical Center, Shanghai Jiao Tong University School of Medicine, Dongfang Road 1678#, Pudong district, Shanghai, China.
Sci Rep. 2025 May 8;15(1):16043. doi: 10.1038/s41598-025-01180-2.
Intervertebral disc degeneration (IDD) is a prevalent cause of low back pain, significantly impacting health worldwide. While IDD is associated with aging, its precise molecular mechanisms remain inadequately understood, limiting the development of targeted therapies. Nucleus pulposus cells (NPCs) are crucial to maintaining disc integrity and are central to understanding IDD progression. This study used single-cell and bulk RNA sequencing to dissect the cellular landscape and gene expression profiles in IDD. By analyzing these data, we identified distinct NPC subtypes and their roles in the degenerative disc microenvironment. Pseudotime and cellular communication network analyses further elucidated the temporal progression and signaling interactions of NPCs during disc degeneration. Four critical genes-TCF19, GDF15, RNMT, and C12orf45-were identified as significantly upregulated in IDD. TCF19 emerged as a key gene in the transitional states of NPCs, suggesting its pivotal role in IDD progression. In vivo experiments using a rat model indicated that Tcf19 knockdown significantly mitigated disc degeneration, reducing both abnormal collagen deposition and inflammation markers. This study unveils the complex molecular dynamics within IDD, providing new insights into distinct NPC subtypes and key genetic players. TCF19, in particular, holds promise as a therapeutic target for IDD. Our findings lay the groundwork for developing targeted treatment strategies, potentially improving the management and outcomes for individuals suffering from disc degeneration.
椎间盘退变(IDD)是导致腰痛的常见原因,对全球健康产生重大影响。虽然IDD与衰老相关,但其确切的分子机制仍未得到充分了解,这限制了靶向治疗的发展。髓核细胞(NPCs)对于维持椎间盘完整性至关重要,并且是理解IDD进展的核心。本研究使用单细胞和批量RNA测序来剖析IDD中的细胞格局和基因表达谱。通过分析这些数据,我们确定了不同的NPC亚型及其在退变椎间盘微环境中的作用。伪时间和细胞通讯网络分析进一步阐明了椎间盘退变过程中NPCs的时间进展和信号相互作用。四个关键基因——TCF19、GDF15、RNMT和C12orf45——被确定在IDD中显著上调。TCF19成为NPCs过渡状态的关键基因,表明其在IDD进展中的关键作用。使用大鼠模型的体内实验表明,Tcf19基因敲低显著减轻了椎间盘退变,减少了异常胶原沉积和炎症标志物。本研究揭示了IDD内复杂的分子动态,为不同的NPC亚型和关键基因参与者提供了新的见解。特别是,TCF19有望成为IDD的治疗靶点。我们的研究结果为制定靶向治疗策略奠定了基础,可能改善椎间盘退变患者的管理和治疗效果。