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Scoliosis and Spinal Disorders: Molecular Biomarkers and Therapeutic Strategies

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 October 2026 | Viewed by 695

Editor


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Guest Editor
Third Department of Orthopaedic Surgery, “KAT”-Hospital and Medical School, National and Kapodistrian University of Athens, Athens, Greece
Interests: molecular signaling in orthopaedic diseases; pathophysiology of osteoarthritis; biomarkers and pathological background of non-union fractures; bone metabolism basis of fragility fractures and management; pathophysiology and molecular basis of spinal deformities and spinal cord Injuries
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Special Issue Information

Dear Colleagues,

Recent research has unveiled significant findings regarding intracellular signaling events during Scoliotic and Spinal deformities’ development and progression in several pathologies. Current studies focus on the microscopic and macroscopic examination of the contribution of several molecules, such as cytokines, chemokines, growth factors, protein receptors and hormones, in intracellular signal transduction cascades. They aim to reveal potential therapeutic targets for the prevention and management of Scoliotic and Spinal disorders, along with biomarker indices to characterize the disease severity and effectiveness of the applied treatment. Nevertheless, the complexity of the molecular processes involved in Scoliotic and Spinal deformities’ pathogenesis and progression means that they remain little understood.

This Special Issue of CIMB aims to provide preclinical and clinical evidence on the pathophysiology of Spinal diseases and demonstrate potential therapeutic or diagnostic applications based on recent experimental advancements. Original research and review articles will be considered if they clearly add value to the available body of literature. These articles’ thematic scope should comprise the clinical, diagnostic, prognostic and therapeutic aspects of these disorders and their molecular background.

The topics of interest include, but are not limited to, the following:

  • In vitro experimental discoveries regarding the molecular signaling in Scoliosis and other Spinal deformities;
  • The results from in vivo and animal model experiments investigating the functional role of intracellular molecules;
  • Examinations of the expression of cytokines or growth factors that may be used as biomarkers for prognostic or diagnostic purposes;
  • Studies that investigate the relationship between Spinal deformities’ clinical characteristics and specific biochemical pathways;
  • Potential target therapies for the management of Scoliosis and Spinal malformations;
  • The metabolic basis of Scoliosis progression.

We look forward to receiving your contributions.

Dr. Angelos Kaspiris
Guest Editor

Manuscript Submission Information

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Keywords

  • intracellular interactions during the progression of spinal disorders
  • molecular signaling in scoliosis
  • growth factor expression in spinal disorders and deformities
  • biomarkers
  • molecular-driven treatment

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Published Papers (1 paper)

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Research

24 pages, 39283 KB  
Article
Titer- and Intervention Timing-Dependent Functional Effects of AAV9-NeuroD1 Gene Therapy on Spinal Cord Injury
by Alex Roman, Maggie Sorensen, Ezequiel Marron Fernandez de Velasco, Ann M. Parr, Andrew W. Grande and Walter C. Low
Curr. Issues Mol. Biol. 2026, 48(8), 786; https://doi.org/10.3390/cimb48080786 - 2 Aug 2026
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Abstract
Spinal cord injury (SCI) often results in varying degrees of motor and sensory dysfunction with limited potential for recovery. Research into in vivo astrocyte-to-neuron reprogramming has led to promising results that, if translated to SCI, could offer substantial therapeutic benefit by replenishing lost [...] Read more.
Spinal cord injury (SCI) often results in varying degrees of motor and sensory dysfunction with limited potential for recovery. Research into in vivo astrocyte-to-neuron reprogramming has led to promising results that, if translated to SCI, could offer substantial therapeutic benefit by replenishing lost populations of neurons for functional restoration. Previous studies have shown that AAV9-mediated delivery of NeuroD1 is capable of reprogramming astrocytes into neurons in vivo after chronic SCI in rats. Here we evaluate the dose-dependent functional and neuroprotective potential of the NeuroD1 gene therapy platform for acute and subacute SCI in rats. The Cre-dependent, DIO-based AAV9-NeuroD1 gene therapy platform was administered directly into the spinal cord of female Long-Evans rats after moderate, thoracic level 8/9 contusion SCI at one of two intervention timepoints: immediately after injury (acute) or 1 week post-contusion (subacute). The viruses were administered at a titer of 1011 or 1013 GC/mL. We demonstrate that the AAV9-NeuroD1 reprogramming platform successfully, albeit variably, transduced spinal cells that persisted up to 6 weeks post-injury. However, histological analysis revealed substantial neuronal off-targeting, suggesting a lack of astrocyte-specific targeting from the AAV9 DIO-based delivery platform. Surprisingly, we also found titer- and intervention timing-dependent effects on motor function and tissue preservation—as demonstrated by 1–2 point decrease in BBB scoring and near 50% increase in peak lesion cavitation area—when AAV9-NeuroD1 was administered immediately after SCI. While did not find any effects of the AAV9-NeuroD1 platform on sensory function or neuroinflammatory cell density, a subset of NeuroD1 signal reflected phagocytic uptake by Iba1 and CD68-expressing microglia/macrophages. These results indicate that the NeuroD1 reprogramming platform can exacerbate injury-related functional deficits when administered in the acute stage of injury, but has neuroprotective benefit on tissue preservation when administered in the subacute stage of injury. Our study demonstrates that several factors must be considered, including viral titer and intervention timing, to assess the therapeutic potential of AAV9-NeuroD1-mediated reprogramming for SCI. Full article
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