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Molecular and Cellular Mechanisms of Spinal Cord Injury and Repair
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Molecular and Cellular Mechanisms of Spinal Cord Injury and Repair

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 31 August 2025 | Viewed by 4429

Special Issue Editor

Dr. Victoria Moreno-Manzano

E-Mail Website
Guest Editor
Neuronal and Tissue Regeneration Laboratory, Centro de Investigación Príncipe Felipe (CIPF), Valencia, Spain
Interests: spinal cord injury repair; cell and gene therapy; biomaterials; neural stimulation

Special Issue Information

Dear Colleagues,

Spinal cord injury (SCI) is a devastating, debilitating, and life-altering condition that currently lacks a cure or effective treatment. After SCI, the descending and ascending communication from the brain to the peripheral sensors and vice versa are abruptly altered. Because of the primary trauma and the consequent secondary damage and loss of innervation, a cascade of degenerating and adaptive responses is activated. The main goal of this Special Issue is to focus on collecting new advances describing the molecular and cellular mechanisms involved in the SCI pathological process, as well as adaptative spontaneous responses and therapeutical approaches. Novel transcriptional regulations, funtional neuronal, glial, or other infiltrated cell entity responses, or therapeutical molecular or cellular experimental approaches will highly contribute to better defining the molecular and cellular scenario of the injured spinal cord and the consequent structural and funtional adaptive process.

Dr. Victoria Moreno-Manzano
Guest Editor

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Keywords

  • spinal cord injury
  • molecular changes
  • neuronal degeneration
  • circuit regeneration
  • transcriptomics
  • cell imaging
  • single-cell analysis
  • cell communication
  • behavior
  • functional outputs

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Published Papers (5 papers)

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Research

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14 pages, 2128 KiB  
Article
Montelukast Improves Urinary Bladder Function After Complete Spinal Cord Injury in Rats
by Elena E. Keller, Sophina Bauer, Karin Roider, Michael Kleindorfer, Peter Törzsök, Julia Tevini, Thomas Felder, Ludwig Aigner and Lukas Lusuardi
Int. J. Mol. Sci. 2025, 26(12), 5606; https://doi.org/10.3390/ijms26125606 - 11 Jun 2025
Viewed by 40
Abstract
Bladder dysfunction is among the most drastic and quality-of-life-reducing conditions after spinal cord injury (SCI). Neuroinflammation in the lower urinary tract (LUT) after SCI could be a key driver of neurogenic bladder dysfunction and tissue fibrosis. Leukotrienes, a group of highly active lipid [...] Read more.
Bladder dysfunction is among the most drastic and quality-of-life-reducing conditions after spinal cord injury (SCI). Neuroinflammation in the lower urinary tract (LUT) after SCI could be a key driver of neurogenic bladder dysfunction and tissue fibrosis. Leukotrienes, a group of highly active lipid mediators, are potent inflammatory mediators. Here, we explored the potential of early montelukast (MLK) therapy, a cysteinyl leukotriene receptor 1 antagonist, on LUT function and structure four weeks after severe SCI in rats. Rats (strain Lewis, female, n = 50) received a permanent bladder catheter, followed by a complete T9 spinal cord transection. MLK was given daily, starting on day one post-injury. Bladder and locomotor function were regularly assessed. Bladder tissue was histologically and immunhistochemically analyzed. Post-SCI, MLK concentrations in plasma and cerebrospinal fluid were clinically relevant. MLK improved bladder functionality. MLK had no impact on smooth muscle alignment and uroepithelial integrity at this early SCI time point. This pilot study gave first insights into early, continuous oral MLK treatment with the first promising results of preserved LUT function and possible subsequent improved tissue integrity. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Spinal Cord Injury and Repair)
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25 pages, 3399 KiB  
Article
Reanalysis of Published Histological Data Can Help to Characterize Neuronal Death After Spinal Cord Injury
by Pablo Ruiz-Amezcua, Nadia Ibáñez-Barranco, David Reigada, Irene Novillo, Altea Soto, María Asunción Barreda-Manso, Teresa Muñoz-Galdeano, Rodrigo M. Maza, Francisco J. Esteban and Manuel Nieto-Díaz
Int. J. Mol. Sci. 2025, 26(8), 3749; https://doi.org/10.3390/ijms26083749 - 16 Apr 2025
Viewed by 1364
Abstract
Neuronal death is a central event in spinal cord injury (SCI) pathophysiology. Despite its importance, we have a fragmentary vision of the process. In our opinion, the research community has accumulated enough information to provide a more detailed, integrated vision of neuronal death [...] Read more.
Neuronal death is a central event in spinal cord injury (SCI) pathophysiology. Despite its importance, we have a fragmentary vision of the process. In our opinion, the research community has accumulated enough information to provide a more detailed, integrated vision of neuronal death after SCI. This work embeds this vision by creating an open repository to store and share data and results from their analysis. We have employed this repository to upload raw images of spinal cord sections from a mouse model of contusive SCI and used this information to compare manual-, threshold-, and neural network-based neuron identifications and to explore neuronal death at the injury penumbra 21 days after injury and the effects of the anti-apoptotic drug ucf-101. Results indicate that, whereas the three identification methods assayed yield coherent estimates of the total number of neurons per section, neural network (NN) outperforms the other two methods. Combining NN identification and image registration has allowed us to characterize neuron distribution among Rexed laminae in the mice T11, revealing spatial patterns in the neuronal death that follows injury and in their survival following ucf-101 treatment. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Spinal Cord Injury and Repair)
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14 pages, 5933 KiB  
Article
Long-Term 5-HT1A Receptor Agonist NLX-112 Treatment Improves Functional Recovery After Spinal Cord Injury
by Ching-Yi Lin, Kevin Li, Thomas Gitchell and Yu-Shang Lee
Int. J. Mol. Sci. 2025, 26(1), 239; https://doi.org/10.3390/ijms26010239 - 30 Dec 2024
Viewed by 856
Abstract
Spinal cord injury (SCI) results in functional deficits below the injured spinal level. The descending serotonergic system in the spinal cord is critically involved in the control of motor and autonomic functions. Specifically, SCI damages the projections of serotonergic fibers, which leads to [...] Read more.
Spinal cord injury (SCI) results in functional deficits below the injured spinal level. The descending serotonergic system in the spinal cord is critically involved in the control of motor and autonomic functions. Specifically, SCI damages the projections of serotonergic fibers, which leads to reduced serotonin inputs and increased amounts of spinal serotonergic receptors. Our previous pharmacological study demonstrated that brief administration of a highly selective 5-HT1A receptor agonist, NLX-112, improves lower urinary tract (LUT) function at the termination stage of thoracic 8 (T8) contusive SCI in rats. However, whether chronic activation of serotonin 5-HT1A receptors by NLX-112 after SCI is beneficial remains an unanswered question. Here, we evaluated the efficacy of long-term NLX-112 intervention starting from two weeks post-T8 contusive SCI for an additional six weeks. We evaluated locomotion, LUT function, bladder morphology, and the number of spinal 5-HT1A receptors in both L4 and L6/S1 spinal cord segments. Our results indicate that NLX-112 treatment significantly improves locomotion in a dose-dependent fashion, improves LUT function, reduces bladder weight and bladder wall thickness, and reduces the SCI-upregulated spinal 5-HT1A receptors compared to vehicle-treated SCI animals. These data suggest promising therapeutic potential for long-term NLX-112 activation of 5-HT1A receptors to treat SCI. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Spinal Cord Injury and Repair)
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14 pages, 5581 KiB  
Article
Noggin-Loaded PLA/PCL Patch Inhibits BMP-Initiated Reactive Astrogliosis
by James Hawes, Ana Gonzalez-Manteiga, Kendall P. Murphy, Marina Sanchez-Petidier, Victoria Moreno-Manzano, Bedika Pathak, Kristin Lampe, Chia-Ying Lin, Jose L. Peiro and Marc Oria
Int. J. Mol. Sci. 2024, 25(21), 11626; https://doi.org/10.3390/ijms252111626 - 29 Oct 2024
Cited by 2 | Viewed by 1154
Abstract
Myelomeningocele (MMC) is a congenital birth defect of the spine and spinal cord, commonly treated clinically through prenatal or postnatal surgery by repairing the unclosed spinal canal. Having previously developed a PLA/PCL polymer smart patch for this condition, we aim to further expand [...] Read more.
Myelomeningocele (MMC) is a congenital birth defect of the spine and spinal cord, commonly treated clinically through prenatal or postnatal surgery by repairing the unclosed spinal canal. Having previously developed a PLA/PCL polymer smart patch for this condition, we aim to further expand the potential therapeutic options by providing additional cellular and biochemical support in addition to its mechanical properties. Bone morphogenetic proteins (BMPs) are a large class of secreted factors that serve as modulators of development in multiple organ systems, including the CNS. We hypothesize that our smart patch mitigates the astrogenesis induced, at least partly, by increased BMP activity during MMC. To test this hypothesis, neural stem or precursor cells were isolated from rat fetuses and cultured in the presence of Noggin, an endogenous antagonist of BMP action, with recombinant BMPs. We found that the developed PLA/PCL patch not only serves as a biocompatible material for developing neural stem cells but was also able to act as a carrier for BMP–Notch pathway inhibitor Noggin, effectively minimizing the effect of BMP2 or BMP4 on NPCs cultured with the Noggin-loaded patch. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Spinal Cord Injury and Repair)
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Review

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20 pages, 2299 KiB  
Review
Mechanisms of Different Motor Neurons in the Occurrence of Spasticity After Spinal Cord Injury: A Narrative Review
by Han Gong, Ze-Yan Zhang, Zhi-Xuan Duan, Xin-Ao Mao, Yuan-Yuan Wu, Jia-Sheng Rao and Xiao-Xia Du
Int. J. Mol. Sci. 2025, 26(11), 5162; https://doi.org/10.3390/ijms26115162 - 28 May 2025
Viewed by 280
Abstract
Spasticity is a common complication after spinal cord injury (SCI) that significantly diminishes quality of life and complicates daily management. As a hallmark of upper motor neuron lesions, spasticity emerges through a complex post-injury process involving the resolution of spinal shock, an imbalance [...] Read more.
Spasticity is a common complication after spinal cord injury (SCI) that significantly diminishes quality of life and complicates daily management. As a hallmark of upper motor neuron lesions, spasticity emerges through a complex post-injury process involving the resolution of spinal shock, an imbalance between excitatory and inhibitory signaling, and maladaptive neuronal plasticity, leading to hyperreflexia and chronic spasticity. Severe spasticity frequently results in pain, sleep disturbances, and marked functional impairments. This review systematically integrates motor neuron alterations with corresponding muscle manifestations, providing a comprehensive analysis of the brain–spinal cord–muscle pathway in spasticity pathogenesis. Through an in-depth analysis of the pathological and physiological changes in motor neurons post-SCI, this review offers a novel perspective that unveils the intrinsic mechanisms underlying spasticity formation, thereby establishing a robust theoretical foundation for developing targeted therapeutic strategies. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Spinal Cord Injury and Repair)
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