Objective Lumbar disc herniation is among the most common and disabling spinal disorders, driven by the interplay of mechanical overload, structural failure, and cellular dysfunction. Despite advances in surgical interventions, achieving true biological repair of herniated discs remains a major clinical challenge. This review aims to critically examine the biomechanical landscape of disc herniation, focusing on how altered load transmission, tissue stiffness, and structural disruption influence cellular behavior and tissue regeneration. It further explores mechanobiological mechanisms governing repair and highlights emerging biomimetic models and technologies that integrate mechanical and biological insights to promote functional disc restoration.
Methods A comprehensive literature review was conducted using the Web of Science Core Collection, PubMed (National Library of Medicine), and ScienceDirect databases. The search was limited to peer-reviewed journal articles published in English and focused on studies related to lumbar disc herniation.
Results While decades of research have elucidated the biomechanical factors contributing to disc herniation, recent advances in mechanobiology have uncovered how mechanical cues influence cellular behavior, tissue repair, and degeneration. Evidence suggests that true disc regeneration cannot be achieved through biological replacement or mechanical stabilization alone; rather, it requires restoring functional biomechanics, specifically, the disc’s ability to sense, adapt to, and sustain physiological loading.
Conclusion Viewing disc herniation through a mechanobiological lens offers new opportunities to develop targeted therapies aimed at restoring both tissue integrity and load-bearing functionality, paving the way for more effective regenerative interventions.
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This study aimed to elucidate the efficacy and safety of mesenchymal stromal cell (MSC) therapy for chronic discogenic low back pain (LBP). A systematic literature search was conducted on PubMed/Medline, Scopus, Cochrane, and ClinicalTrials.gov following PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-analysis) guidelines. Eligible studies included published and ongoing clinical trials assessing intradiscal MSC injections in patients with chronic discogenic LBP unresponsive to conservative treatment. Risk-of-bias (RoB) assessment was performed through MINORS (Methodological Index for Non-randomized Studies) and RoB 2 tools. Within- and between-group differences were expressed as means and 95% confidence intervals. Effect sizes were calculated through Cohen d and g. Data from 10 published clinical studies (n=736; 470 in treatment and 266 in control groups) revealed a mean age of 41.5 years and an average follow-up of 21.6 (range, 6–72) months. Various MSC sources were employed, including autologous and allogeneic bone marrow-derived MSCs and adipose-derived MSCs, with doses ranging from 6×10⁶ to over 50×10⁶ cells/disc. Visual analogue scale, Oswestry Disability Index, and quality-of-life questionnaires indicated modest improvements in pain, disability, and functional status. Additionally, magnetic resonance imaging assessments occasionally demonstrated increased disc hydration and stabilization or improvement of Pfirrmann grade. Data from 8 ongoing trials (n=498 participants; 276 treatment, 222 control) with follow-up periods ranging 6–24 months further corroborate the feasibility and safety of MSC-based interventions. MSC therapy is a biologically-driven approach for managing chronic discogenic LBP. While preliminary data support its potential to alleviate pain and improve disc integrity, further high-quality, standardized trials are necessary to optimize treatment protocols and confirm long-term clinical benefits.
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Objective Regeneration of corticospinal tract (CST) axons after spinal cord injury (SCI) is a key element in rebuilding neuronal connections to restore voluntary motor function. However, it remains challenging owing to limited effective interventions. This study adopted a modified transcranial optogenetic technique to stimulate CST axon regeneration into the injury site of completely transected SCI and explore the underlying molecular mechanisms.
Methods A novel optogenetic light emitting diode (LED) device was used to stimulate the brain motor cortex in channelrhodopsin-2–yellow fluorescent protein (ChR2-YFP) transgenic mice to observe the regeneration of CST axons in the injury site of a complete SCI. The LED device was also used In vitro to stimulate the motor cortex slices of the transgenic mouse brain for observing the outgrowth of their neurites.
Results After transcranial optogenetic stimulation, the pyramidal neurons of bilateral cerebral motor cortices, in ChR2-YFP transgenic mice were activated, CST axons regenerated into the injury site of the spinal cord, and the motor function of the paralyzed hindlimbs improved. Proteomic analysis revealed that CST axon regeneration was associated with the activation of the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) pathway in the cerebral motor cortices. In vitro LED blue light illumination enhanced the outgrowth of neurites from the brain slices of transgenic mice. Treatment with a JAK2/STAT3 inhibitor led to a significant attenuation of neurite outgrowth.
Conclusion The modified transcranial optogenetic technique stimulated bilateral motor cortices, in the brains of ChR2-YFP transgenic mice. It increased the excitability of pyramidal neurons in the motor cortices, and promoted CST axon regeneration by activating the JAK2/STAT3 pathway, repairing complete SCI.
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Objective Herein, we investigated whether mesenchymal stem cells (MSCs) transplantation combined with electroacupuncture (EA) treatment could decrease the proportion of proinflammatory microglia/macrophages and neurotoxic A1 reactive astrocytes and inhibit glial scar formation to enhance axonal regeneration after spinal cord injury (SCI).
Methods Adult rats were divided into 5 groups after complete transection of the spinal cord at the T10 level: a control group, a nonacupoint EA (NA-EA) group, an EA group, an MSC group, and an MSCs+EA group. Immunofluorescence labeling, quantitative real-time polymerase chain reaction, enzyme-linked immunosorbent assay, and Western blots were performed.
Results The results showed that MSCs+EA treatment reduced the proportion of proinflammatory M1 subtype microglia/macrophages, but increased the differentiation of anti-inflammatory M2 phenotype cells, thereby suppressing the mRNA and protein expression of proinflammatory cytokines (tumor necrosis factor-α and IL-1β) and increasing the expression of an anti-inflammatory cytokine (interleukin [IL]-10) on days 7 and 14 after SCI. The changes in expression correlated with the attenuated neurotoxic A1 reactive astrocytes and glial scar, which in turn facilitated the axonal regeneration of the injured spinal cord. In vitro, the proinflammatory cytokines increased the level of proliferation of astrocytes and increased the expression levels of C3, glial fibrillary acidic protein, and chondroitin sulfate proteoglycan. These effects were blocked by administering inhibitors of ErbB1 and signal transducer and activator of transcription 3 (STAT3) (AG1478 and AG490) and IL-10.
Conclusion These findings showed that MSCs+EA treatment synergistically regulated the microglia/macrophage subpopulation to reduce inflammation, the formation of neurotoxic A1 astrocytes, and glial scars. This was achieved by downregulating the ErbB1-STAT3 signal pathway, thereby providing a favorable microenvironment conducive to axonal regeneration after SCI.
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Neurospine 2022;19(2):272-280. Published online June 30, 2022
Objective To comprehensively characterize the utilization of alginate hydrogels as an alternative treatment modality for spinal cord injury (SCI).
Methods An extensive review of the published literature on studies using alginate hydrogels to treat SCI was performed. The review of the literature was performed using electronic databases such as PubMed, EMBASE, and OVID MEDLINE electronic databases. The keywords used were “alginate,” “spinal cord injury,” “biomaterial,” and “hydrogel.”
Results In the literature, we identified a total of 555 rat models that were treated with alginate scaffolds for regenerative biomarkers. Alginate hydrogels were found to be efficient and promising substrates for tissue engineering, drug delivery, neural regeneration, and cellbased therapies for SCI repair. With its ability to act as a pro-regenerative and antidegenerative agent, the alginate hydrogel has the potential to improve clinical outcomes.
Conclusion The emerging developments of alginate hydrogels as treatment modalities may support current and future tissue regenerative strategies for SCI.
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This is a review article examining the pharmacologic and regenerative cell therapy for spinal cord injury. A literature search during last 10 years were conducted using key words. Case reports, experimental (nonhuman) studies, papers other than English language were excluded. Up-to-date information on the pharmacologic and regenerative cell therapy for spinal cord injury was reviewed and statements were produced to reach a consensus in 2 separate consensus meeting of WFNS Spine Committee. The statements were voted and reached a consensus using Delphi method. Pharmacologic and regenerative cell therapy for spinal cord injury have long been an interest of many experimental and clinical researches. Clinical studies with methylpredinisolone have not shown clear cut benefit. Other drugs such as Rho inhibitor, minocycline, riluzole, granulocyte colony-stimulating factor have also been tried without significant benefits. Regenerative cell therapy using different types of stem cells, different inoculation techniques, and scaffolds have undergone many trials highlighting the efficacies of cells and their limitations. This review article summarizes the current knowledge on pharmacologic and regenerative cell therapy for spinal cord injury. Unfortunately, there is a need for further experimental and human trials to recommend effective pharmacologic and regenerative cell therapy.
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Intervertebral disc degeneration is the primary cause of back pain and associated with neurological disorders including radiculopathy, myelopathy, and paralysis. The currently available surgical treatments predominantly include the excision of pathological discs, resulting in the function loss, immobilization, and potential additional complications due to the altered biomechanics. Gene therapy approach involves gene transfer into cells, affects RNA and protein synthesis of the encoded genes in the recipient cells, and facilitates biological treatment. Relatively long-exerting therapeutic effects by gene therapy are potentially advantageous to treat slow progressive degenerative disc disease. In gene therapy, the delivery method and selection of target gene(s) are essential. Although gene therapy was first mediated by viral vectors, technological progress has enabled to apply nonviral vectors and polyplex micelles for the disc. While RNA interference successfully provides specific downregulation of multiple genes in the disc, clustered regularly interspaced short palindromic repeats (CRISPR) system has increased attention to alter the process of intervertebral disc degeneration. Then, more recent findings of our studies have suggested autophagy, the intracellular self-digestion, and recycling system under the negative regulation by the mammalian target of rapamycin (mTOR), as a gene therapy target in the disc. Here we briefly review backgrounds and applications of gene therapy for the disc, introducing strategies of autophagy and mTOR signaling modulation through selective RNA interference.
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Low back pain remains a highly prevalent pathology engendering a tremendous socioeconomic burden. Low back pain is generally associated with intervertebral disc (IVD) degeneration, a process involving the deterioration of nucleus pulpous (NP) cells and IVD matrix. Scientific interest has directed efforts to restoring cell numbers as a strategy to enable IVD regeneration. Currently, mesenchymal stromal cells (MSCs) are being explored as cell therapy agents, due to their easy accessibility and differentiation potential. For enhancement of MSCs, growth factor supplementation is commonly applied to induce differentiation towards a chondrogenic (NP) cell phenotype. The wnt signaling pathways play a crucial role in chondrogenesis, nonetheless, literature appears to present controversies with regard to wnt3a and wnt5a for the induction of NP cells, chondrocytes, and MSCs. This review aims to summarize the reporting on wnt3a/wnt5a mediated NP cell differentiation, and to elucidate the mechanisms involved in wnt3a and wnt5a mediated chondrogenesis for potential application as cell therapy supplements for IVD regeneration. Our review suggests that wnt3a, subsequently replaced with a chondrogenic stimulating growth factor, can enhance the chondrogenic potential of MSCs in vitro. Contrariwise, wnt5a is suggested to play a role in maintaining cell potency of differentiated NP or chondrogenic cells.
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Spinal cord injury (SCI), with an incidence rate of 246 per million person-years among adults in Taiwan, remains a devastating disease in the modern day. Elderly men with lower socioeconomic status have an even higher risk for SCI. Despite advances made in medicine and technology to date, there are few effective treatments for SCI due to limitations in the regenerative capacity of the adult central nervous system. Experiments and clinical trials have explored neuro-regeneration in human SCI, encompassing cell- and molecule-based therapies. Furthermore, strategies have aimed at restoring connections, including autologous peripheral nerve grafts and biomaterial scaffolds that theoretically promote axonal growth. Most molecule-based therapies target the modulation of inhibitory molecules to promote axonal growth, degrade glial scarring obstacles, and stimulate intrinsic regenerative capacity. Among them, acidic fibroblast growth factor (aFGF) has been investigated for nerve repair; it is mitogenic and pluripotent in nature and could enhance axonal growth and mitigate glial scarring. For more than 2 decades, the authors have conducted multiple trials, including human and animal experiments, using aFGF to repair nerve injuries, including central and peripheral nerves. In these trials, aFGF has shown promise for neural regeneration, and in the future, more trials and applications should investigate aFGF as a neurotrophic factor. Focusing on aFGF, the current review aimed to summarize the historical evolution of the utilization of aFGF in SCI and nerve injuries, to present applications and trials, to summarize briefly its possible mechanisms, and to provide future perspectives.
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