To elucidate the pathological significance of acid-sensing ion channels (ASICs) in intervertebral disc degeneration (IVDD), the database of Medline, Web of Science, and EmBase were carefully screened. Search terms used in each database varied slightly to optimize results. Data relating to the correlation between ASICs and IVDD was systematically collected and integrated into the review. 11 basic science studies, containing the related information, were finally identified for inclusion. Intervertebral disc degeneration (IVDD) is a common disease in middle-aged and elderly people, which has a great impact on patients’ quality of life. Many research teams have attempted to elucidate the pathogenesis of this degenerative disease, and have made considerable progress. Acid-sensing ion channels (ASICs) were once reported to be able to regulate the apoptosis process of chondrocytes in joint cartilage, which has been transplanted into the IVDD-related research. ASIC1a functions as the mediator for cells in nucleus pulposus (NP) and endplate (EP), with whose activation the apoptosis process would be accelerated. Moreover, ASIC1a’s activation could also regulate the anabolism in chondrocytes of EP, facilitating the degeneration. ASIC3 would only promote the degeneration in NP, possibly via its pro-inflammatory effect. The distribution of ASICs in NP, EP, annulus fibrosus, and the particular functions of ASIC1a and ASIC3 remind us about the pathological significance of ASICs in IVDD, which could be a promising therapeutic target in future treatment for IVDD.

为了阐明酸敏感离子通道（ASICs）在椎间盘退变（IVDD）中的病理学意义，仔细筛选了Medline，Web of Science和EmBase的数据库。每个数据库中使用的搜索词略有不同，以优化结果。系统地收集了与ASIC和IVDD之间的相关性相关的数据，并将其整合到审查中。最终确定了包含相关信息的11项基础科学研究。椎间盘退变（IVDD）是中老年人常见病，对患者的生活质量影响很大。许多研究团队已经尝试阐明这种退行性疾病的发病机理，并取得了长足的进步。曾经有报道称酸敏感离子通道（ASICs）能够调节关节软骨中软骨细胞的凋亡过程，现已移植到IVDD相关研究中。ASIC1a充当髓核（NP）和终板（EP）中细胞的介体，通过它们的激活可以加快凋亡过程。此外，ASIC1a的活化还可以调节EP软骨细胞的合成代谢，从而促进变性。ASIC3仅可能通过其促炎作用促进NP的变性。ASIC在NP，EP，纤维环中的分布以及ASIC1a和ASIC3的特殊功能使我们想起了IVDD中ASIC的病理学意义，这可能成为IVDD未来治疗的有希望的治疗靶点。已被移植到IVDD相关的研究中。ASIC1a充当髓核（NP）和终板（EP）中细胞的介体，通过它们的激活可以加快凋亡过程。此外，ASIC1a的活化还可以调节EP软骨细胞的合成代谢，从而促进变性。ASIC3仅可能通过其促炎作用促进NP的变性。ASIC在NP，EP，纤维环中的分布以及ASIC1a和ASIC3的特殊功能使我们想起了IVDD中ASIC的病理学意义，这可能成为IVDD未来治疗的有希望的治疗靶点。已被移植到IVDD相关的研究中。ASIC1a充当髓核（NP）和终板（EP）中细胞的介体，通过它们的激活可以加快凋亡过程。此外，ASIC1a的活化还可以调节EP软骨细胞的合成代谢，从而促进变性。ASIC3仅可能通过其促炎作用促进NP的变性。ASIC在NP，EP，纤维环中的分布以及ASIC1a和ASIC3的特殊功能使我们想起了IVDD中ASIC的病理学意义，这可能成为IVDD未来治疗的有希望的治疗靶点。通过其激活，细胞凋亡过程将被加速。此外，ASIC1a的活化还可以调节EP软骨细胞的合成代谢，从而促进变性。ASIC3仅可能通过其促炎作用促进NP的变性。ASIC在NP，EP，纤维环中的分布以及ASIC1a和ASIC3的特殊功能使我们想起了IVDD中ASIC的病理学意义，这可能成为IVDD未来治疗的有希望的治疗靶点。通过其激活，细胞凋亡过程将被加速。此外，ASIC1a的活化还可以调节EP软骨细胞的合成代谢，从而促进变性。ASIC3仅可能通过其促炎作用促进NP的变性。ASIC在NP，EP，纤维环中的分布以及ASIC1a和ASIC3的特殊功能使我们想起了IVDD中ASIC的病理学意义，这可能成为IVDD未来治疗的有希望的治疗靶点。