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Peripheral Neuropathies: Molecular Research and Novel Therapy—2nd Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: 20 September 2025 | Viewed by 603

Special Issue Editor

Special Issue Information

Dear Colleagues,

The quality of life of those with peripheral neuropathies is undermined by their various symptoms, such as pain and numbness of the extremities, muscle weakness, and autonomic disorders. The neuropathies are caused by gene mutations, immune system disorders, metabolic abnormalities, cancers and anti-cancer drugs, and other systemic diseases; however, the onset and progression mechanisms remain largely unclear and the efficacious remedies against them have not yet been developed. This Special Issue provides a platform for researchers pursuing the molecular pathogenesis of peripheral neuropathies and novel therapeutic approaches toward them. Detailed information is available from the findings of recent research on inherited neuropathy (e.g., Charcot–Marie–Tooth disease, hereditary ATTR amyloidosis, and Fabry disease), diabetic polyneuropathy, immune-mediated neuropathy (e.g., Guillain–Barré syndrome, chronic inflammatory demyelinating polyneuropathy, and autoimmune autonomic ganglionopathy), and drug-induced neuropathy (e.g., anti-cancer drugs including immune checkpoint inhibitors, amiodarone, and tumor necrosis factor-a antagonists). Basic studies regarding axonal degeneration, demyelination, and neuron–Schwann cell interplay under physiological and pathophysiological conditions are also welcome for submission.

Dr. Zhidong Zhou
Guest Editor

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Keywords

  • axonal degeneration
  • demyelination
  • schwann cells
  • dorsal root ganglia
  • diabetic neuropathy
  • chemotherapy-induced peripheral neuropathies
  • immune-mediated neuropathies
  • immune checkpoint inhibitors
  • charcot-marie-tooth disease
  • autonomic neuropathies

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Published Papers (1 paper)

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Research

18 pages, 3515 KiB  
Article
Potassium/Sodium Citrate Attenuates Paclitaxel-Induced Peripheral Neuropathy
by Daisuke Uta, Hideki Nakamura, Kengo Maruo, Kanoko Matsumura, Yohei Usami and Toshiaki Kume
Int. J. Mol. Sci. 2025, 26(7), 3329; https://doi.org/10.3390/ijms26073329 - 3 Apr 2025
Viewed by 386
Abstract
Chemotherapy-induced peripheral neuropathy (CIPN) is a significant adverse event with unclear mechanisms and limited treatment alternatives. This study aimed to investigate the efficacy of two alkalizing agents, a mixture of potassium citrate and sodium citrate (K/Na citrate) or sodium bicarbonate (NaHCO3), [...] Read more.
Chemotherapy-induced peripheral neuropathy (CIPN) is a significant adverse event with unclear mechanisms and limited treatment alternatives. This study aimed to investigate the efficacy of two alkalizing agents, a mixture of potassium citrate and sodium citrate (K/Na citrate) or sodium bicarbonate (NaHCO3), in preventing and treating paclitaxel (PTX)-induced mechanical allodynia in rodents. The results from rodent models demonstrated that repeated prophylactic administration of K/Na citrate or NaHCO3 could inhibit the development of PTX-induced mechanical allodynia. Moreover, K/Na citrate was effective in preventing the PTX-induced exacerbation of mechanical allodynia, even when treatment was initiated immediately after the onset of allodynia. K/Na citrate also reduced the levels of the plasma complement component anaphylatoxin C3a in a PTX-induced CIPN rat model. Complement activation, resulting in the production of C3a, has been implicated in the pathogenesis of this model. Additionally, pretreatment with Na citrate significantly prevented the reduction in neurite outgrowth caused by PTX. Furthermore, K/Na citrate inhibited spontaneous and mechanical stimuli-induced firing in spinal dorsal horn neurons. These findings indicate that K/Na citrate may regulate the development of PTX-induced mechanical allodynia by modulating complement activation and providing neuroprotection against PTX-induced peripheral nerve injury. This study implies that alkalization could help prevent PTX-induced peripheral neuropathy and mitigate its exacerbation. Full article
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