ArticleJournal of orthopaedic surgery and research2024
Repetitive transcranial magnetic stimulation promotes motor function recovery in mice after spinal cord injury via regulation of the Cx43-autophagy loop.
Article in Journal of orthopaedic surgery and research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The Dual Role of Connexins in Stroke, Neurotrauma, Neurodegenerative and Psychiatric Disorders: A Global Systematic Review.Molecules (Basel, Switzerland) · 2026Pooled it
- Magnetic fields as biophysical activators of autophagy: A preclinical systematic review.Biochemistry and biophysics reports · 2026Review
- Simulated closed-loop magnetic stimulation promotes function recovery and axonal regeneration in spinal cord injury.Communications biology · 2026Article
- Magnetically Responsive Piezoelectric Nanocapacitors Enhance Neural Recovery Following Spinal Cord Injury via Targeted Spinal Magnetic Stimulation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Emerging strategies for spinal cord injury repair: stem cells, extracellular vesicles, biomaterials, and neuromodulation.Frontiers in bioengineering and biotechnology · 2026Review
- Roles and regulatory mechanisms of autophagy in the pathology of spinal cord injury.Burns & trauma · 2026Review
- Translating a Preclinically Tested 15 Hz rTMS Protocol to Humans With Chronic Spinal Cord Injury: A Safety and Feasibility Study.Annals of clinical and translational neurology · 2025Article
- The Concomitant Effect of the Antiepileptic Drug Lacosamide and rTMS on an SH-SY5Y Model of Neuronal Excitability.Neurology international · 2025Article
- Transcranial iTBS Combined With Trans-Spinal iTBS Targeting PDE1A/cAMP/PKA Axis Regulates Neural Regeneration After Spinal Cord Injury.CNS neuroscience & therapeutics · 2025Article
- Role of astrocytes connexins - pannexins in acute brain injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
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Authors and funding
6 authors.
Funding
Abstract
Spinal cord injury (SCI) is a severe condition with an extremely high disability rate. It is mainly manifested as the loss of motor, sensory and autonomic nerve functions below the injury site. High-frequency transcranial magnetic stimulation, a recently developed neuromodulation method, can increase motor function in mice with spinal cord injury. This study aimed to explore the possible mechanism by which transcranial magnetic stimulation (TMS) restores motor function after SCI. A complete T8 transection model of the spinal cord was established in mice, and the mice were treated daily with 15 Hz high-frequency transcranial magnetic stimulation. The BMS was used to evaluate the motor function of the mice after SCI. Western blotting and immunofluorescence were used to detect the expression of Connexin43 (CX43) and autophagy-related proteins in vivo and in vitro, and correlation analysis was performed to study the relationships among autophagy, CX43 and motor function recovery after SCI in mice. Western blotting was used to observe the effect of magnetic stimulation on the expression of mTOR pathway members. In the control group, the expression of CX43 was significantly decreased, and the expression of microtubule-associated protein 1 A/1b light chain 3 (LC3II) and P62 was significantly increased after 4 weeks of spinal cord transection. After high-frequency magnetic stimulation, the level of CX43 decreased, and the levels of LC3II and P62 increased in primary astrocytes. The BMS of the magnetic stimulation group was greater than that of the control group. High-frequency magnetic stimulation can inhibit the expression of CX43, which negatively regulates autophagic flux. HF-rTMS increased the expression levels of mTOR, p-mTOR and p-S6. Our experiments showed that rTMS can restore hindlimb motor function in mice after spinal cord injury via regulation of the Cx43-autophagy loop and activation of the mTOR signalling pathway.
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