Modern treatments for degenerative disc diseases of the lumbosacral spine. A literature review

Konovalov, N A; Nazarenko, A G; Asyutin, D S; Zelenkov, Petr; Onoprienko, R A; Korolishin, V A; Cherkiev, I U; Martynova, M A; Закиров, Б А; Тimonin, S Yu; Kosyrkova, Alexandra; Pimenova, L. F.; Pogosyan, A.; Batyrov, A A

doi:10.17116/neiro2016804102-108

Cited by 24 publications

(7 citation statements)

References 33 publications

(27 reference statements)

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“…It is estimated that ~84% of people will experience LBP during their lives worldwide, with 10% becoming chronically disabled (1), thus seriously affecting quality of life and imposing heavy economic burdens on families and society. Currently, clinical interventions for IDD primarily include conservative medication and surgery (spinal fusion or total disc replacement); however, these treatments are only able to temporarily relieve pain symptoms, without solving the underlying issues in IDD and providing a permanent cure (2,3). Therefore, it is necessary to deeply investigate the underlying mechanisms of IDD, in order to develop more effective strategies for preventing and treating IDD-associated LBP.…”

Section: Introductionmentioning

confidence: 99%

lncRNA/circRNA‑miRNA‑mRNA ceRNA network in lumbar intervertebral disc degeneration

et al. 2019

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accumulating evidence has indicated that noncoding rnas are involved in intervertebral disc degeneration (idd); however, the competing endogenous rna (cerna)-mediated regulatory mechanisms in idd remain rarely reported. The present study aimed to comprehensively investigate the alterations in expression levels of circular rna (circrna), long noncoding rna (lncrna), microrna (mirna/mir) and mrna in the nucleus pulposus (nP) of patients with idd. in addition, crucial lncrna/circrna-mirna-mrna cerna interaction axes were screened using the GSe67567 microarray dataset obtained from the Gene expression omnibus database. after data preprocessing, differentially expressed circrnas (decs), lncrnas (dels), mirnas (deMs) or genes (deGs) between IDD and normal controls were identified using the linear Models for Microarray data method. a protein-protein interaction (PPi) network was constructed for deGs based on protein databases, followed by module analysis. The cerna network was constructed based on the interaction between mirnas and mrnas, and lncrnas/circrnas and mirnas. The underlying functions of mrnas were predicted using the database for annotation, Visualization and integrated Discovery database. The present study identified 636 DECs, 115 dels, 84 deMs and 1,040 deGs between patients with idd and control individuals. PPi network analysis demonstrated that Fos proto-oncogene, aP-1 transcription factor subunit (FoS), mitogen-activated protein kinase 1 (MaPK1), hypoxia inducible factor 1 subunit α (HiF1a) and transforming growth factor β1 (TGFB1) were hub genes and enriched in modules. Metastasis-associated lung adenocarcinoma transcript 1 (MalaT1)/hsa_circrna_102348-hsa-mir-185-5p-TGFB1/FoS, MalaT1-hsa-mir-155-5p-HiF1a, hsa_circrna_102399-hs a-mir-302a-3p-HiF1a, MalaT1-hsa-mir-519d-3p-MaPK1 and hsa_circrna_100086-hsa-mir-509-3p-MaPK1 cerna axes were obtained by constructing the cerna networks. in conclusion, these identified ceRNA interaction axes may be crucial targets for the treatment of idd.

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Section: Introductionmentioning

confidence: 99%

lncRNA/circRNA‑miRNA‑mRNA ceRNA network in lumbar intervertebral disc degeneration

et al. 2019

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“…There are many inducing factors for IDD, including genetics, ageing and gender. At present, the clinical interventions for IDD mainly include conservative drug therapy and surgery [ 8 ]. However, the existing treatment options can not solve the problem fundamentally, but only temporarily alleviate the pain.…”

Section: Introductionmentioning

confidence: 99%

Ginsenoside Rg1 inhibits nucleus pulposus cell apoptosis, inflammation and extracellular matrix degradation via the YAP1/TAZ pathway in rats with intervertebral disc degeneration

Yang

et al. 2022

J Orthop Surg Res

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Purpose Intervertebral disc degeneration (IDD) is one of the main causes of low back pain, which not only affects patients’ life quality, but also places a great burden on the public health system. Recently, ginsenoside Rg1 has been found to act in IDD; however, the mechanism is still unclear. The purpose of this study is to explore the function of ginsenoside Rg1 and its molecular mechanism in IDD. Methods The rat model of IDD and nucleus pulposus (NP) experimental groups treated with ginsenoside Rg1 was constructed for investing the role of ginsenoside Rg1 in IDD rats. In the in vitro and in vivo study, the histological morphological changes, motor threshold (MT), inflammatory factors, oxidative stress, apoptosis and expression of the YAP1/TAZ signaling pathway-related proteins of the intervertebral discs (IVD) were measured by histological staining, mechanical and thermal stimulation, ELISA, qRT-PCR, flow cytometry, and western blot, respectively. Results Ginsenoside Rg1 significantly increased the threshold for mechanical and thermal stimulation and alleviated histological changes in IDD rats. Ginsenoside Rg1 had a significant inhibitory effect on the secretion level of inflammatory factors, redox activity, extracellular matrix (ECM) degradation in IVD tissue and NP cells, and apoptosis in NP cells. Further investigation revealed that ginsenoside Rg1 significantly inhibited the expression of YAP1/TAZ signaling pathway-related proteins. Additionally, the above inhibitory effect of ginsenoside Rg1 on IDD progression was concentration-dependent, that is, the highest concentration of ginsenoside Rg1 was most effective. Conclusion Ginsenoside Rg1 inhibits IDD progression by suppressing the activation of YAP1/TAZ signaling pathway. This means that ginsenoside Rg1 has the potential to treat IDD.

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“…IDD is featured by the reduction of NP and degradation of proteoglycan, Aggrecan, and collagen in the extracellular matrix (ECM), which disrupts the homeostasis of NP and shifts IVD maintenance toward degeneration and catabolism (Wang et al, 2015). The current clinical interventions for IDD mainly include conservative medication and surgery (spinal fusion or total disk replacement); nevertheless, these therapeutic approaches only temporarily relieve the pain symptoms, instead of providing a permanent cure (Konovalov et al, 2016;Zhu et al, 2019). Hence, developing novel and potent therapies for patients with IDD remains an urgent issue to be solved.…”

Section: Introductionmentioning

confidence: 99%

Bone Mesenchymal Stem Cells Promote Extracellular Matrix Remodeling of Degenerated Nucleus Pulposus Cells via the miR-101-3p/EIF4G2 Axis

Zeng

Xiao-lin

Cao

et al. 2021

Front. Bioeng. Biotechnol.

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The etiology of lumbocrural pain is tightly concerned with intervertebral disk degeneration (IDD). Bone mesenchymal stem cell (BMSC)-based therapy bears potentials for IDD treatment. The properties of microRNA (miRNA)-modified BMSCs may be altered. This study investigated the role and mechanism of BMSCs promoting extracellular matrix (ECM) remodeling of degenerated nucleus pulposus cells (NPCs) via the miR-101-3p/EIF4G2 axis. NPCs were collected from patients with IDD and lumbar vertebral fracture (LVF). The expressions of miR-101-3p and ECM-related proteins, Collagen-I (Col-I) and Collagen-II (Col-II), were detected using the reverse transcription-quantitative polymerase chain reaction. The expressions of Col-I and Col-II, major non-collagenous component Aggrecan, and major catabolic factor Matrix metalloproteinase-13 (MMP-13) were detected using Western blotting. BMSCs were cocultured with degenerated NPCs from patients with IDD. Viability and apoptosis of NPCs were measured using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and flow cytometry. After the degenerated NPCs were transfected with the miR-101-3p inhibitor, the expressions of ECM-related proteins, cell viability, and apoptosis were detected. The targeting relationship between miR-101-3p and EIF4G2 was verified. Functional rescue experiments verified the effects of miR-101-3p and EIF4G2 on ECM remodeling of NPCs. Compared with the NPCs of patients with LVF, the degenerated NPCs of patients with IDD showed downregulated miR-101-3p, Col-II, and Aggrecan expressions and upregulated MMP-13 and Col-I expressions. BMSCs increased the expressions of miR-101-3p, Aggrecan, and Col-II, and decreased the expressions of MMP-13 and Col-I in degenerated NPCs. BMSCs enhanced NPC viability and repressed apoptosis. Downregulation of miR-101-3p suppressed the promoting effect of BMSCs on ECM remodeling. miR-101-3p targeted EIF4G2. Downregulation of EIF4G2 reversed the inhibiting effect of the miR-101-3p inhibitor on ECM remodeling. In conclusion, BMSCs increased the miR-101-3p expression in degenerated NPCs to target EIF4G2, thus promoting the ECM remodeling of NPCs.

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Modern treatments for degenerative disc diseases of the lumbosacral spine. A literature review

Cited by 24 publications

References 33 publications

lncRNA/circRNA‑miRNA‑mRNA ceRNA network in lumbar intervertebral disc degeneration

lncRNA/circRNA‑miRNA‑mRNA ceRNA network in lumbar intervertebral disc degeneration

Ginsenoside Rg1 inhibits nucleus pulposus cell apoptosis, inflammation and extracellular matrix degradation via the YAP1/TAZ pathway in rats with intervertebral disc degeneration

Bone Mesenchymal Stem Cells Promote Extracellular Matrix Remodeling of Degenerated Nucleus Pulposus Cells via the miR-101-3p/EIF4G2 Axis

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