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Molecular Advances in Combinatorial Therapies for Spinal Cord Injury

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: 20 August 2025 | Viewed by 1611

Special Issue Editor


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Guest Editor
Indiana University School of Medicine, Indianapolis, IN, USA
Interests: spinal cord injury; neural plasticity; neuroinflammation; bladder dysfunction

Special Issue Information

Dear Colleagues,

Spinal cord injury (SCI) leads to severe functional deficits, necessitating the exploration of efficient treatment strategies. Single treatment approaches have shown limited efficacy in improving function, prompting the adoption of combinatory strategies. These strategies leverage a combination of therapeutic interventions, including cell transplantation, stem cell programming therapy, rehabilitation, engineering, and pharmacological approaches, to target multiple aspects of SCI pathology simultaneously. By integrating these approaches, synergistic effects may enhance functional recovery more effectively than individual treatments alone. Additionally, high-throughput technologies have been employed to elucidate the underlying pathological mechanisms of SCI and evaluate the therapeutic effects of novel interventions. Integrating these advanced technologies with combinatory treatment approaches holds promise for optimizing SCI management and improving patient outcomes. This Special Issue aims to highlight recent advancements in combinatory treatment strategies alongside high-throughput technologies for SCI, providing insights into the development of effective therapeutic interventions. Data on molecular mechanisms or pathophysiology are essential, and papers that only contain clinical trials/data will not be accepted.

Dr. Lingxiao Deng
Guest Editor

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Keywords

  • molecular
  • cellular
  • engineering
  • spinal cord injury

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Published Papers (1 paper)

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Research

18 pages, 11425 KiB  
Article
Mitochondrial Cardiolipin-Targeted Tetrapeptide, SS-31, Exerts Neuroprotective Effects Within In Vitro and In Vivo Models of Spinal Cord Injury
by Baylen Ravenscraft, Do-Hun Lee, Heqiao Dai, Abbie Lea Watson, Gabriela Inés Aparicio, Xianlin Han, Ling-Xiao Deng and Nai-Kui Liu
Int. J. Mol. Sci. 2025, 26(7), 3327; https://doi.org/10.3390/ijms26073327 - 2 Apr 2025
Viewed by 495
Abstract
Spinal cord injury (SCI) affects millions globally, leading to severe motor and sensory deficits with no effective clinical treatment. Cardiolipin (CL), a mitochondria-specific phospholipid, plays a critical role in bioenergetics and apoptosis. Emerging evidence suggests that CL alterations contribute to secondary SCI pathology, [...] Read more.
Spinal cord injury (SCI) affects millions globally, leading to severe motor and sensory deficits with no effective clinical treatment. Cardiolipin (CL), a mitochondria-specific phospholipid, plays a critical role in bioenergetics and apoptosis. Emerging evidence suggests that CL alterations contribute to secondary SCI pathology, but their precise role and underlying mechanisms remain fully understudied. In this study, we investigated the protective effects of SS-31 on CL alteration, neuronal death, tissue damage, and behavioral recovery after SCI using both in vitro and in vivo models, lipidomics analysis, histological evaluation, and behavioral assessments. In vitro investigations used primary spinal cord neuron cultures, challenged with either rotenone or glutamatergic excitotoxicity, with protective capabilities measured via cell death assays and neurite morphological analysis. In vivo investigations used female adult C57Bl/6 mice, challenged with a contusive SCI. The results showed that SS-31 reduced rotenone- and glutamate-induced mitochondrial dysfunction and neuronal death in a dose-dependent manner in vitro. Additionally, SS-31 attenuated rotenone- and glutamate-induced neurite degeneration in vitro. Lipidomics analysis revealed a reduction in CL at 24 h post-SCI in adult mice, which was attenuated by SS-31 in a dose-dependent manner. Consistent with this effect, SS-31 improved behavioral recovery after SCI in adult mice, although it had no significant effect on tissue damage. These findings suggest that CL alteration may play a key role in the pathogenesis of SCI, at least in the C57BL/6 mouse, and as such could be an attractive therapeutic target for ameliorating secondary SCI. Full article
(This article belongs to the Special Issue Molecular Advances in Combinatorial Therapies for Spinal Cord Injury)
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