Selected Ion Channels in Chemotherapy-Induced Peripheral Neuropathy: Mechanisms and Translational Limits
- 1Acupuncture and Tuina School, Chengdu University of Traditional Chinese Medicine, No. 37, Shierqiao Road, Chengdu 610075, China
Abstract
Chemotherapy-induced peripheral neuropathy (CIPN) combines abnormal sensory firing with neuronal and axonal injury. This critical narrative review focuses on selected voltage-gated sodium, calcium, and Kv7 potassium channels and transient receptor potential channels in chemotherapy-specific systems and human studies. Acute modulation is distinguished from altered channel abundance or localization and persistent remodeling. Human axonal-excitability studies support membrane dysfunction during acute oxaliplatin neurotoxicity but do not identify a sodium-channel subtype. Experimental studies identify changes in trafficking, stimulus sensitivity, and current that vary by time and compartment. Clinical analgesia does not itself demonstrate channel engagement or axonal protection. Duloxetine provides a symptomatic benchmark; results for channel-directed drugs and cannabinoid formulations remain inconsistent or design-limited. Natural products are treated as defined pharmacological examples, not as ranked candidates. A six-domain reporting template links target identity, potency, exposure, selectivity, CIPN context, and safety without assigning a composite score or evidence grade. Translation requires matching channel pharmacology to achievable unbound exposure and testing symptom relief separately from preservation of axons and protective sensation.
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BibTeX
@article{zhang2026selected,
title = {{Selected Ion Channels in Chemotherapy-Induced Peripheral Neuropathy: Mechanisms and Translational Limits}},
author = {Xunlang Zhang and Dekun Liu and Mingkai Yu and Ruibin Zhang and Lingling Liu and Jinyan Liu and Xiaojing Liu and Yingjie Wang and Shuguang Yu and Sha Yang},
journal = {Biomolecules},
year = {2026},
month = oct,
doi = {10.3390/biom16101502},
url = {https://www.mdpi.com/2218-273X/16/10/1502},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Selected Ion Channels in Chemotherapy-Induced Peripheral Neuropathy: Mechanisms and Translational Limits
AU - Xunlang Zhang
AU - Dekun Liu
AU - Mingkai Yu
AU - Ruibin Zhang
AU - Lingling Liu
AU - Jinyan Liu
AU - Xiaojing Liu
AU - Yingjie Wang
AU - Shuguang Yu
AU - Sha Yang
PY - 2026
DA - 2026/10/15
JO - Biomolecules
DO - 10.3390/biom16101502
UR - https://www.mdpi.com/2218-273X/16/10/1502
AB - Chemotherapy-induced peripheral neuropathy (CIPN) combines abnormal sensory firing with neuronal and axonal injury. This critical narrative review focuses on selected voltage-gated sodium, calcium, and Kv7 potassium channels and transient receptor potential channels in chemotherapy-specific systems and human studies. Acute modulation is distinguished from altered channel abundance or localization and persistent remodeling. Human axonal-excitability studies support membrane dysfunction during acute oxaliplatin neurotoxicity but do not identify a sodium-channel subtype. Experimental studies identify changes in trafficking, stimulus sensitivity, and current that vary by time and compartment. Clinical analgesia does not itself demonstrate channel engagement or axonal protection. Duloxetine provides a symptomatic benchmark; results for channel-directed drugs and cannabinoid formulations remain inconsistent or design-limited. Natural products are treated as defined pharmacological examples, not as ranked candidates. A six-domain reporting template links target identity, potency, exposure, selectivity, CIPN context, and safety without assigning a composite score or evidence grade. Translation requires matching channel pharmacology to achievable unbound exposure and testing symptom relief separately from preservation of axons and protective sensation.
SN - 2218-273X
ER -