Growth Factors in Intervertebral Disc Homeostasis

Intervertebral disc degeneration is a complex age-related pathology associated with back pain. Research on the growth factors that regulate disc homeostasis is of critical importance for understanding the basis of the disease. Here we summarize the data on the expression and function of various growth factors in the disc from in vivo and in vitro studies, as well as on their alterations during degeneration and ageing. Such studies are becoming more crucial in the prospect of clinical application of growth factors for the treatment of disc degeneration.     

生长因子治疗椎间盘退变的研究进展

目的：探讨椎间盘退变的发生机制,总结生长因子治疗椎间盘退变的相关研究成果,并提出尚待解决的问题和未来研究的热点。方法：从刺激椎间盘细胞增殖,促进椎间盘基质的合成,抑制椎间盘细胞的凋亡,应用方式,现阶段研究中存在的问题等方面对国内外相关研究进行总结。结果：使用生长因子治疗椎间盘退变可以从生理结构上阻止、逆转椎间盘退变,恢复椎间盘丢失的高度和生物学功能。结论：椎间盘的生长因子治疗尚存在一定的问题和不足,随着研究的深入和应用方法的改进,生长因子治疗有望为椎间盘退变提供一条新的治疗途径。     

椎间盘退行性变的相关生物分子因素

背景：随着年龄的增长,椎体过度活动和超负荷承载使椎体加快出现老化,并在外力的作用下,继发病理性改变,以致椎间盘纤维环破裂,椎间盘内的髓核突出,引起腰腿痛和神经功能障碍。 目的：总结椎间盘退行性变的相关生物分子因素的研究进展,并展望其发展趋势。 方法：应用计算机检索PubMed数据库;中国知网数据库;万方数据库;维普数据库2000-02/2012-01有关椎间盘退行性变的相关生物分子因素的文献。检索文献包括研究原著及综述,排除重复性研究。 结果与结论：共保留32篇文献归纳总结。椎间盘退变是由多种相关因素在长期条件下相互作用而引起的,是一系列脊柱退行性病变的前提和慢性病理过程的基础。椎间盘髓核细胞不仅是残留脊索细胞,而且对于整个椎间盘功能的维持起到重要作用。对髓核细胞在RNA、DNA及蛋白水平相关生物分子因素的研究,为延缓及治疗以及将来扭转和修复椎间盘退行性变提供了可能。     

腰椎间盘退变的分子病理学变化及发病机制

背景：腰椎间盘退变是引起腰腿痛的常见原因,椎间盘退变的病理改变及发病机制至今仍未完全明确。 目的：介绍腰椎间盘退变的分子病理改变及其发病机制的研究进展。 方法：以“disc histology,disc degenerative disease,disc gene”等主题词检索PubMed数据库,检索时间为2005/2010年,筛选与腰椎间盘组织学变化和发病机制相关的文献,总结归纳腰椎间盘退变的研究进展和研究结果。 结果与结论：共检索到与腰椎间盘退变有关的文章118篇,共纳入30篇。结果表明腰椎间盘退变受多种因素影响,包括基因遗传因素、自然老化和积累性损伤等,基因的多形性是诱发退变的重要前置因素。椎间盘退变可通过免疫反应、机械性压迫或不稳定、血循环障碍和炎性递质等因素导致椎间盘退变性疾病。老化和病理性退变在影像和病理上难以区别,应根据椎间盘退变性疾病的具体情况采取合理的治疗方法,生物学治疗提供了新的治疗思路,但目前仍处在实验研究阶段。     

The cell biology of intervertebral disc aging and degeneration

Intervertebral disc degeneration, which mimics disc aging but occurs at an accelerated rate, is considered to be related to neck or low back pain and disc herniation. Degenerated discs show breakdown of the extracellular matrix and thus fail to bear the daily loadings exerted on the spine. Rather than a passive process of wear and tear, disc degeneration is an aberrant, cell-mediated response to progressive structural failure due to aging and other environmental factors such as abnormal mechanical stress. With aging and degeneration, disc cells undergo substantially biologic changes, including alternation of cell type in the nucleus pulposus, increased cell density but decreased number of viable cells as a result of increased cell death and increased cell proliferation, increased cell senescence, and altered cell phenotype which is characterized by compromised capability of synthesizing correct matrix components and by enhanced catabolic metabolism. These changes are involved in the process of disc degeneration through the complicated interactions among them. To retard or reverse disc degeneration, the abnormal conditions of the decreased viable cell population and the altered cell phenotype should be corrected. As potential therapies for disc degeneration, intradiscal protein injection, gene transfer and cell implantation are being understudied in vivo. Suppression of excessive apoptosis and accelerated senescence of disc cells may be other choices for treating disc degeneration. When performing a biologic therapy in order to repair or regenerate the degenerated disc, nutrient and biomechanical factors should also be incorporated, because they are the major causes of the biologic changes experienced by disc cells. Moreover, a very early intervention is indicated by the finding that the onset of human disc degeneration occurs as early as by adolescence.     

椎间盘退变模型的研究现状及进展

目的：探讨椎间盘退变模型的研究现状及进展。方法：在Pubmed、中国知网查阅有关椎间盘退变模型研究的文献,进行汇总分析。结果：椎间盘退变模型可以通过体外和体内两种方法构建,前者包括椎间盘细胞模型和椎间盘组织模型,后者包括诱发性椎间盘退变模型和自发性椎间盘退变模型。体外模型适用面较广,但培养要求较高,不能全面模拟体内环境;体内培养干预技术较容易实现,但适用面较窄。结论：人椎间盘退变的影响因素繁多,目前的椎间盘退变模型往往具有一定的局限性,无法全面地模拟出人的椎间盘退变情况。无创、微创构建椎间盘退变模型将是未来的发展趋势。     

退行性变椎间盘组织转化生长因子β1基因的表达

背景：据报道,转化生长因子β1能促进椎间盘细胞的增殖与分化,并参与其损伤修复过程。但转化生长因子β1是否参与椎间盘退变的过程？ 目的：分析在人体退行性变椎间盘组织中转化生长因子β1的表达情况,并探讨其与人体椎间盘退行性变的关系。 方法：收集正常椎间盘组织30例,退行性变人体椎间盘组织530例,采用苏木精-伊红染色、免疫印迹和RT-PCR方法进行研究,对退行性变的椎间盘组织进行病理学分型,分别检测转化生长因子β1在不同类型退变的椎间盘中表达的情况并与正常椎间盘组织进行对比分析。 结果与结论：苏木精-伊红染色病理学诊断：将退行性变的椎间盘组织根据病理学改变程度分为4型。免疫印迹法和RT-PCR法均显示：在正常和退变椎间盘组织中,转化生长因子β1均有表达,但在病变组织中随病变加重转化生长因子β1表达量随之增加,退变组织与正常组织比较差异有非常显著性意义 (P < 0.01)。说明转化生长因子β1高表达与人体椎间盘退行性变呈正相关。     

软骨终板形态与椎间盘退变的相关性

背景：以往研究证明多种内环境因素共同作用引发椎间盘退变,最重要的机制为椎间盘软骨终板的退变。 目的：分析椎间盘退变与终板形态的关系。 方法：回顾性分析62例因椎间盘源性慢性下腰痛和79例因髓核脱出致神经根性症状患者的腰椎MRI正中矢状位图像资料。根据腰椎MRI正中矢状位T1W1图像确定终板形态,T2W1图像确定椎间盘退变程度分级。 结果与结论：平坦型和不规则型终板最常见于椎间盘退变人群下腰椎,L5/S1平坦型最多见。髓核脱出组与椎间盘源性慢性下腰痛组中凹陷型终板椎间盘退变程度均较平坦型、不规则型低,平坦型终板椎间盘退变程度较不规则型低(P < 0.01)。两组间凹陷型与不规则型终板椎间盘退变程度差异无显著性意义,髓核脱出组平坦型椎间盘退变程度较椎间盘源性慢性下腰痛组高(P < 0.05)。提示随着椎间盘退变程度的加重,软骨终板形态有由凹陷型向平坦型、不规则型依次转变的趋势。     

脊柱椎间盘退变与高尿酸血症的相关性

背景:高尿酸血症是常见的代谢性疾病,高尿酸血症患者以尿酸结晶形成导致痛风为主要临床表现。既往研究仅报道了尿酸结晶会导致脊柱椎间盘的退变,但关于高尿酸血症与脊柱椎间盘退变的相关性研究较少。目的:回顾性分析高尿酸血症患者脊柱椎间盘的退变特点以及血尿酸浓度与脊柱椎间盘退变的相关性。方法:回顾性分析2021年1月至2022年12月在西南医科大学附属医院骨科就诊并被诊断为脊柱椎间盘退变的所有患者,纳入97例高尿酸血症患者作为高尿酸血症组,然后根据性别、年龄按照1∶2进行匹配,将194例非高尿酸血症患者作为对照组。收集两组患者的血尿酸检验结果,并在全脊柱MRI图像上对两组患者的椎间盘退变程度进行Pfirrmann评分。比较两组患者椎间盘退变程度的差异,分析血尿酸浓度与椎间盘退变程度的相关性。结果与结论:①高尿酸血症组的椎间盘退变程度Pfirrmann评分大于对照组,且高尿酸血症组的椎间盘退变总数大于对照组,差异均有显著性意义(P<0.05);②Spearman相关分析显示,在高尿酸血症组内的多个节段,男性患者的椎间盘退变程度与血尿酸浓度呈正相关(C_(3/4):r=0.317,C_(4/5):r=0.333,C_(5/6):r=0.309,L_(2/3):r=0.443;P<0.05);女性患者的椎间盘退变程度也与血尿酸浓度呈正相关(C_(3/4):r=0.354,C_(4/5):r=0.388,C_(6/7):r=0.312,T_(7/8):r=0.282,T_(9/10):r=0.305,T_(11/12):r=0.277,L_(4/5):r=0.319,L_(5)-S_(1):r=0.367,P<0.05);③在对照组中,男性和女性患者的椎间盘退变程度与血尿酸浓度无明显相关性(P>0.05);④结果提示:在高尿酸血症患者中,血尿酸浓度越高,椎间盘退变程度越严重。因此,高尿酸血症是导致椎间盘退变的危险因素之一。     

Genetics of intervertebral disc disease: A review

Intervertebral disc disease (IVDD) is a common musculoskeletal disease affecting about 5% of all individuals. It is characterized by lumbar disc herniation, which causes nerve root irritation, either mechanically or via inflammatory mediators, and results in radiating pain, known as sciatica. Numerous studies have been conducted to identify the causes and risk factors for IVDD. Lifting heavy loads, torsional stress, and motor vehicle driving are among the best-identified environmental risk factors. However, it has become evident recently from family and twin studies that genetic factors may also be important in IVDD. This hypothesis was strengthened by the identification of two collagen IX alleles associated with sciatica and lumbar disc herniation. In addition, disc degeneration has been shown to be related to an aggrecan gene polymorphism, a Vitamin D receptor and matrix metalloproteinase-3 gene alleles. This review highlights the genetic role and occupational aspects of IVDD.     

Effect of severity of intervertebral disc injury on mesenchymal stem cell-based regeneration

Mesenchymal stem cell (MSC) implantation has been shown previously to arrest disc degeneration. This study aims to assess the effect of severity of disc degeneration on the ability of MSCs to arrest the degeneration. Disc degeneration was induced in New Zealand white rabbits at lumbar levels by annular puncture. The degeneration was allowed to progress for 1 month (early group) or 7 months (late group), followed by intradiscal injection of autologous MSCs. For disc levels that received MSCs treatment, 1 x 10(5) BrdU-labeled MSCs were injected per disc level. For the early group, MSC-injection had no significant effects on disc height or the progression of disc degeneration. For the late group, although the MSC-injected discs displayed lower disc heights than the control discs, they were significantly less degenerated together with near normal level of proteoglycan in localized areas. This is the first pilot study to demonstrate that severity of degeneration can influence the therapeutic effect of MSCs. Future studies of cell-based intervertebral disc regeneration should be carefully controlled in the context of stage of disc degeneration.     

Intraoperative malposition of pedicle probe or screws: a potential cause of the acceleration of degeneration in superior adjacent intervertebral disc

Adjacent segment degeneration (ASD) is considered as a long-term complication of spinal fusion procedure. Numerous clinical studies have reported some factors related with ASD, but few could address the reason why the incidence of caudal ASD is significantly lower than that of cranial ASD. Because the pedicle of vertebral arch is closer to the superior endplate of vertebrea and its cranial intervertebral disc, there might be some possibilities of malpositions of pedicle probe or screws into the superior vertebral endplate or disc during the procedure of posterior intervertebral fusion. A number of evidences have showed that puncture of intervertebral disc will result in disc degeneration. Thus the authors put forward the hypothesis that intraoperative malposition of pedicle probe or screws might be a cause of ASD at cranial segments.     

腰椎间盘退变与局部转化生长因子β1及炎性细胞因子的关系

背景：近年来随着椎间盘退变分子水平研究的不断进展,转化生长因子β1基因在椎间盘细胞的增殖分化过程中具有一定作用,且参与了椎间盘的损伤修复过程,但转化生长因子β1是否也参与了椎间盘退变的病理生理过程目前尚无定论。目的：探讨腰椎间盘退变程度与转化生长因子β1及炎性细胞因子之间的关系。方法：选择72例椎间盘退变患者作为观察组(轻度22例,中度26例,重度24例),30例非椎间盘退变患者作为对照组,检测两组患者椎间盘局部转化生长因子β1及白细胞介素1β、白细胞介素6、白细胞介素8、肿瘤坏死因子α等炎性细胞因子水平,在两组之间及不同椎间盘退变程度患者之间进行对比分析。同时采用直线相关分析法分析转化生长因子β1与炎性细胞因子及腰椎间盘退变的相关性。中国组织工程研究杂志出版内容重点：组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松;组织工程结果与结论：观察组患者腰椎间盘局部转化生长因子β1及白细胞介素1β、白细胞介素6、白细胞介素8、肿瘤坏死因子α等炎性细胞因子水平均显著高于对照组(P < 0.01)。重度退变患者腰椎间盘局部转化生长因子β1及白细胞介素1β、白细胞介素6、白细胞介素8、肿瘤坏死因子α等炎性细胞因子水平显著高于轻度及中度患者(P < 0.01),同时中度患者显著高于轻度患者(P < 0.01)。转化生长因子β1与白细胞介素1β、白细胞介素6、白细胞介素8、肿瘤坏死因子α等炎性细胞因子以及椎间盘退变程度均呈显著正相关(r=0.198,0.312,0.356,0.275,0.724,P < 0.01)。提示转化生长因子β1及白细胞介素1β、白细胞介素6、白细胞介素8、肿瘤坏死因子α等炎性细胞因子在退变椎间盘局部水平增高,且增高程度随着退变严重程度的增加而增加。中国组织工程研究杂志出版内容重点：组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松;组织工程     

Transplantation of mesenchymal stem cells embedded in Atelocollagen gel to the intervertebral disc: a potential therapeutic model for disc degeneration

Intervertebral disc degeneration is considered to be one of the major causes of low back pain. Despite this irreversible phenomenon, attempts to decelerate disc degeneration using various techniques have been reported. However, to date there has been no proven technique effective for broad clinical application. Based on previous studies, we hypothesize that maintenance of proteoglycan content in the disc is achieved by avoiding the depletion of nucleus pulposus and preserving the structure of the annulus is a primary factor in decelerating disc degeneration.One novel approach to solve the dilemma of intervertebral disc degeneration is found at the stem cell level. Mesenchymal stem cells (MSCs) are known to possess the ability to differentiate into various kinds of cells from mesenchymal origin. Although the majority of cells that contribute to disc formation are known to obtain chondrocyte-like phenotypes, no reported study has emphasized the correlation with mesenchymal stem cells.To evaluate the possible potential of MSCs in disc cell research and treatment of degenerative disc disease, autologous MSCs embedded in Atelocollagen gel were transplanted into the discs of rabbits which had undergone a procedure proven to induce degeneration. The results suggest that MSC transplantation is effective in decelerating disc degeneration in experimental models and provided new hopes for treatment of degenerative disc disease in humans. Atelocollagen gel served as an important carrier of MSCs in transplantation, permitting proliferation, matrix synthesis and differentiation of MSCs. This study strengthens the viable efficacy of practical application of MSCs in treatment of intervertebral disc disease.     

脂肪间充质干细胞复合血小板凝胶修复兔椎间盘退变

背景：富含血小板的血浆凝胶作为三维支架使其中干细胞可以呈立体生长,同时富含血小板的血浆凝胶又释放大量生长因子,促进脂肪间充质干细胞增殖及分化。 目的：探讨脂肪间充质干细胞-富含血小板的血浆凝胶复合体注入兔椎间盘退变模型后的修复作用。 方法：取兔动脉血采用二次离心法制备自体富血小板血浆,取兔肩胛间区脂肪分离培养脂肪间充质干细胞,制备脂肪间充质干细胞-富含血小板的血浆凝胶复合体。新西兰大白兔随机分为对照组、模型组、富含血小板的血浆凝胶组和脂肪间充质干细胞-富含血小板的血浆凝胶复合体组,后3组以穿刺法制备椎间盘退变模型,退变模型制备完成2周后,富含血小板的血浆凝胶组和脂肪间充质干细胞-富含血小板的血浆凝胶复合体组分别对退变间盘中注射相应材料。 结果与结论：兔椎间盘退变后,间隙明显降低,髓核信号明显降低,髓核内基质高,密度染色较深;而经富含血小板的血浆凝胶和脂肪间充质干细胞-富含血小板的血浆凝胶复合体治疗后,上述症状明显改善,且脂肪间充质干细胞-富含血小板的血浆凝胶复合体的治疗效果更好。提示对退变椎间盘内注射富含血小板的血浆凝胶支架及脂肪间充质干细胞-富含血小板的血浆凝胶复合体均有利于减少退变对椎间盘的影响,其中脂肪间充质干细胞-富含血小板的血浆凝胶复合体注射效果更为突出。     

腰椎小关节退变的相关因素及生物力学特点

文题释义：腰椎小关节：为相近节段腰椎上位椎体的下关节突与下位椎体的上关节突组成的腰椎后外侧关节,将一个腰椎的椎弓与相邻腰椎的椎弓相连,在腰椎运动中占据着重要的地位。 生物力学：是应用力学原理和方法对生物体中的力学问题定量研究的生物物理学分支,研究范围从生物整体到系统组织,其研究重点是与生理学、医学有关的力学问题。 背景：腰椎小关节退变近年来成为学者们研究的重点,认识腰椎小关节退变的危险因素对于预防以及减少脊柱损害具有关键性作用,并且了解其解剖结构对于治疗脊柱相关疾病及手术实施有着重要的指导意义。 目的：简述腰椎小关节解剖学、组织学特性,总结能够引起腰椎小关节退变的相关危险因素。 方法：利用计算机检索CNKI、万方、维普、PubMed、Elsevier和Web of Science数据库2018年3月至2019年9月有关腰椎小关节退变的文章,检索词为“腰椎小关节,关节囊,关节面方向,神经支配,骨性关节炎,生物力学,下腰痛,椎间盘退变,腰椎滑脱,腰椎退行性脊柱侧弯,lumbar facet joint,joint capsule,articular direction,eneurosis,osteoarthritis,biomechanics,low back pain,intervertebral disc degeneration,umbar spondylolisthesis,lumbar degenerative scoliosis”。查阅相关文章,包括综述、基础研究及临床研究,通过阅读标题及摘要进行初步筛选,排除与主题相关度低的文献,最终共纳入60篇文献进行结果分析。 结果与结论：①腰椎小关节退变的主要危险因素包括年龄、性别、异常应力、关节面方向、关节不对称性、腰椎节段和椎间盘退变;②关节退变后会导致下腰痛、椎间盘退变、腰椎滑脱、退行性脊柱侧弯等临床疾病的发生和发展,严重影响患者的日常生活和工作,降低生活质量。因此,腰椎小关节在脊柱相关疾病的治疗中不应该被忽视。 ORCID: 0000-0002-5700-8674(文王强) 中国组织工程研究杂志出版内容重点：人工关节;骨植入物;脊柱;骨折;内固定;数字化骨科;组织工程     

Understanding embryonic development for cell-based therapies of intervertebral disc degeneration: Toward an effort to treat disc degeneration subphenotypes

Chronic low back and neck pain are associated with intervertebral disc degeneration and are major contributors to the global burden of disability. New evidence now suggests that disc degeneration comprises a spectrum of subphenotypes influenced by genetic background, age, and environmental factors, which may be contributing to the mixed outcomes seen in clinical trials of cell-based therapies that aim to treat disc degeneration. This problem is further compounded by the fact that disc degeneration and aging coincide with an exhaustion of endogenous progenitor cells, imposing limitations on the regenerative capacity of the disc. At the bench-side, current work is focused on applying our knowledge of embryonic disc development to direct and refine differentiation of adult and human-induced pluripotent stem cells into notochord-like and nucleus pulposus-like cells for use in novel cell-based therapies. Accordingly, this review presents the salient features of intervertebral disc development, post-natal maintenance, and regeneration, with emphasis on recent advancements. We also discuss how a stratified approach can be undertaken for the development of future cell-based therapies to bring emerging subphenotypes into consideration.     

水通道蛋白1和3在腰椎间盘退变组织中的表达

背景：腰椎间盘退变由多种因素引起,水通道蛋白变化规律在腰椎间盘退变中的作用研究较少。 目的：比较正常腰椎间盘组织及退变腰椎间盘组织中水通道蛋白1、水通道蛋白3的表达。 方法：收集大理学院附属医院骨科手术切除腰椎爆裂骨折患者腰椎间盘组织15份,退变椎间盘组织15 份,应用苏木精-伊红染色、免疫组织化学染色方法观察水通道蛋白1、水通道蛋白3的表达,测量平均吸光度值。 结果与结论：苏木精-伊红染色结果显示对照组椎间盘组织结构清晰,胶原纤维走形清楚,组织轻微水肿无黏液样变,病例组组织结构模糊紊乱,胶原纤维增生粗大、走行紊乱,组织炎性水肿严重、坏死黏液样变。免疫组织化学方法显示病例组水通道蛋白1、水通道蛋白3平均吸光度值明显低于对照组(P < 0.01),提示水通道蛋白1、水通道蛋白3减少可能是腰椎间盘退变因素之一。     

如何构建能较全面模拟人类椎间盘退变性疾病的椎间盘退变实验动物模型

背景：椎间盘退变性疾病的发病机制目前尚无定论,建立理想的椎间盘退变动物模型是研究该病发病机制或治疗的重要途径。 目的：对近年来各种椎间盘退变动物模型研究的模型选择、建模方法以及优缺点做一综述。 方法：计算机检索万方数据库、知网数据库、PubMed数据库以及FMJS数据库近5年国内外关于椎间盘退变的体内及体外动物模型的文献。 结果与结论：目前的文献报道显示中小型动物是现阶段较为常用的模型动物;造模方法可以分为体内和体外模型两大类,体外模型通过细胞或组织培养,从细胞及分子水平揭示椎间盘退变的机制,体内模型则使用不同种物理或化学方法对椎间盘进行干预,模拟椎间盘退变的结果,并从干预过程中反证椎间盘退变的机制。但因人类的椎间盘退变性疾病发病机制复杂,目前尚无定论,所以目前的动物模型均不能较全面的模拟人类椎间盘退变性疾病。 中国组织工程研究杂志出版内容重点：肾移植;肝移植;移植;心脏移植;组织移植;皮肤移植;皮瓣移植;血管移植;器官移植;组织工程全文链接：     

MicroRNA影响椎间盘退变过程的研究进展及可发展空间

文题释义：miRNA：属于一种受内源性非蛋白质编码调控的单链小分子RNA,可以调控人体近1/3的蛋白编码基因参与机体发育与疾病发生,与许多生物进程的调控密切关联,包括生长发育、细胞增殖、凋亡和分化等。其不仅在许多正常人体发育过程中起着关键作用,而且与多种疾病的发生和发展有关。 自噬：是细胞通过溶酶体吞噬和降解自身细胞质和细胞器的过程。自噬在生长、发育、细胞稳定和成熟分化等方面起着重要作用,作为一种独立的Ⅱ型程序性细胞死亡过程,自噬与细胞凋亡存在着密切关联。 背景：在细胞与分子水平上明确MicroRNA(miRNA)在椎间盘退变过程的作用机制,可为早预防或治疗椎间盘退变继发的一系列脊柱疾患提供新的思路。 目的：综述miRNA在椎间盘退变原因和机制中的研究现状。 方法：应用计算机检索PubMed数据库、万方数据库和中国知网数据库,英文检索词为“miRNA、Intervertebral disc degeneration、Extracellular matrix、Apoptosis、Autophagy、Cartilage endplate、Nucleus pulposus、Fibrous ring”,中文检索词为“miRNA、椎间盘退变、细胞外基质、凋亡、自噬、软骨终板、髓核、纤维环”,最终纳入58篇文章进行综述。 结果与结论：miRNA在椎间盘退变过程中的作用已被广泛研究,部分具体机制得到验证;研究多局限于髓核组织,对软骨终板及纤维环报道较少;随着miRNA深入研究,临床方面的研究仍有较大发展空间。 ORCID: 0000-0002-2312-4255(胡宝阳) 中国组织工程研究杂志出版内容重点：人工关节;骨植入物;脊柱;骨折;内固定;数字化骨科;组织工程