ArticleRedox report : communications in free radical research2025
Redox-dependent activation of protein kinase G1α contributes to transient receptor potential cation channel subfamily V member 1-mediated acute nociceptive pain behavior.
Article in Redox report : communications in free radical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- TRPV1‑mediated central sensitisation: Core mechanisms of migraine chronification and novel targeted therapeutic strategies (Review).International journal of molecular medicine · 2026Review
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8 authors.
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Abstract
backgroundSensory neurons relay the pain signals to the brain via the nociceptive system. Notably, reactive oxygen species (ROS) serve as signaling molecules in the somatosensory system; however, their contribution to sensing noxious stimuli remains poorly understood.
methodsHerein, the role of protein kinase G (PKG)1α, which is highly expressed in sensory neurons and serves as a ROS target, was investigated in sensory neurons in the processing of acute nociceptive pain. Cys42Ser PKG1α-knock-in (PKG1α-KI) mice, devoid of redox-dependent PKG1α activation, were subjected to behavioral testing, ROS detection assays, gene expression experiments, and imaging analyses.
resultsInterestingly, PKG1α-KI mice showed reduced behavioral responses to noxious heat and the transient receptor potential cation channel subfamily V member 1 (TRPV1) agonist capsaicin. Moreover, capsaicin-induced sensory neuron stimulation upregulated ROS production and redox-dependent PKG1α activation. Calcium imaging results and patch-clamp recordings revealed that capsaicin-induced calcium flux and neuronal excitability was reduced in sensory neurons of PKG1α-KI mice.
conclusionAltogether, the findings of this study show the effects of redox-dependent PKG1α activation on capsaicin/TRPV1-mediated signaling in sensory neurons during acute nociceptive pain.
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