Shockwave Therapy Shows Promise in Spinal Cord Injury Repair
Title of Study: Shock waves promote spinal cord repair via TLR3
Authors: Can Gollmann-Tepeköylü, Felix Nägele, Michael Graber, Leo Pölzl, Daniela Lobenwein, Jakob Hirsch, Angela An, Regina Irschick, Bernhard Röhrs, Christian Kremser, Hubert Hackl, Rosalie Huber, Serena Venezia, David Hercher, Helga Fritsch, Nikolaos Bonaros, Nadia Stefanova, Ivan Tancevski, Dirk Meyer, Michael Grimm, Johannes Holfeld
Spinal cord injury (SCI) remains a devastating condition with a poor prognosis and very limited treatment options. Affected patients are severely restricted in their daily activities. Shock wave therapy (SWT) has shown potent regenerative
properties in bone fractures, wounds, and ischemic myocardium via activation of the innate immune receptor TLR3. Here, we report on the efficacy of SWT for the regeneration of SCI. SWT improved motor function and decreased lesion size in WT but not Tlr3–/– mice via inhibition of neuronal degeneration and IL6-dependent recruitment and differentiation of neuronal progenitor cells. Both SWT and TLR3 stimulation enhanced neuronal sprouting and improved neuronal survival, even in human spinal cord cultures. We identified tlr3 as crucial enhancer of spinal cord regeneration in zebrafish. Our findings
indicate that TLR3 signaling is involved in neuroprotection and spinal cord repair and suggest that TLR3 stimulation via SWT could become a potent regenerative treatment option.
Spinal cord injury (SCI) is a severe, often debilitating condition with limited treatment options, leading to restricted mobility and a poor outlook for recovery. Recent findings indicate that shockwave therapy (SWT) might offer new hope for SCI patients by promoting spinal cord regeneration.
This study explored SWT’s regenerative potential in SCI recovery, examining its effects on motor function and spinal cord health in mice. Results showed that SWT improved motor function and reduced lesion size in normal mice. However, in mice lacking the TLR3 gene, a gene involved in immune response and tissue repair—SWT was ineffective, indicating that TLR3 plays a crucial role in SWT’s effectiveness.
The mechanism behind SWT’s success appears to involve TLR3, an immune receptor that activates repair processes in cells. SWT enhanced neuronal survival and sprouting improved neuron connections, stimulating the recruitment and differentiation of neuronal progenitor cells, which are essential for spinal cord repair. These effects were also observed in human spinal cord cultures, suggesting similar benefits could be possible in humans.
Further research in zebrafish identified TLR3 as a key player in spinal cord regeneration, reinforcing its significance in SWT-driven repair. By engaging TLR3, SWT may protect neurons from degeneration and support the growth of new neural pathways, making it a promising candidate for SCI treatment.
In summary, SWT could potentially provide a non-invasive option for SCI repair by enhancing the body’s innate regenerative mechanisms. Further studies are needed, but these findings highlight SWT’s potential as a breakthrough therapy for spinal cord injury.