Polydeoxyribonucleotide Injection as an Alternative to Surgery in Hypoxic Conditions
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To the editor,
I would like to express my sincere appreciation for the detailed discussion of innovative therapeutic approaches for neuropathic pain in the recent article by Joo et al. [1], titled “Adenosine A2A Receptor Agonist, Polydeoxyribonucleotide Treatment Improves Locomotor Function and Thermal Hyperalgesia Following Neuropathic Pain in Rats.” This groundbreaking study not only highlights the efficacy of polydeoxyribonucleotide (PDRN) in improving locomotor function and reducing thermal hyperalgesia, but also demonstrates its regenerative effects on damaged neural tissues.
In line with these findings, our research has further demonstrated the efficacy of PDRN in a different context. We have shown that PDRN significantly promotes tissue repair in experimental models of varicocele, leading to a reduction in testicular necrosis and edema, as well as an improvement in spermatogenesis. These results support the proposal that PDRN, with its regenerative properties, could be a valuable therapeutic option in a variety of medical fields.
PDRN has demonstrated significant potential in enhancing tissue repair and functionality by modulating apoptosis and angiogenesis. In the context of neuropathic pain, PDRN contributes to neuroprotection by reducing apoptotic pathways and promoting anti-inflammatory effects, as evidenced by the downregulation of proinflammatory cytokines such as tumor necrosis factor-α and interleukin-1β. This is particularly important in neuropathic pain, where inflammation and neuronal damage severely impair recovery. Additionally, PDRN’s interaction with the A2A receptor is crucial, as demonstrated by diminished therapeutic effects observed in response to the A2A receptor antagonist 3,7-dimethyl-propargilxanthine (DMPX). This suggests that optimizing PDRN therapy may require careful consideration of receptor interactions [2, 3].
Similarly, in the treatment of varicocele, PDRN contributes to improved testicular function by mitigating hypoxia-induced damage and promoting neoangiogenesis. Hypoxia increases hypoxia-inducible factor 1α expression, leading to elevated vascular endothelial growth factor (VEGF) levels, which are crucial for new blood vessel formation. PDRN further upregulates VEGF expression, thereby increasing microvessel density and reducing apoptosis in testicular tissues. As with diabetic ulcers, this angiogenic effect is also mediated by A2A receptor activation, with diminished outcomes seen after the application of DMPX [4].
The study by Joo et al. [1] also emphasizes the importance of understanding the specific pathways and mechanisms involved in PDRN’s regenerative effects. The modulation of inflammatory mediators and apoptotic pathways, as well as the upregulation of angiogenesis, could serve as key targets for optimizing treatment outcomes. Additionally, we explored the role of inhibitors of apoptosis proteins, such as neuronal apoptosis inhibitory protein (NAIP) and survivin, in regulating apoptosis and spermatogenesis. In experimental varicocele models, PDRN increased NAIP and survivin levels, promoting cell survival and spermatogenesis. However, DMPX reversed these beneficial effects, underscoring the critical role of A2A receptor mediation in PDRN’s mechanism of action [5].
In conclusion, we would like to once again congratulate Joo et al. for their valuable contribution and comprehensive work on the regenerative potential of PDRN in the treatment of neuropathic pain. Their study offers an important foundation for the further exploration of PDRN applications and expands our understanding of this promising therapy. As research progresses, we are confident that PDRN will play an increasingly important role in the management of neuropathic pain and other areas of regenerative medicine.
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Conflicts of Interest
The authors declare no conflict of interest.