ArticleAntioxidants & redox signaling2014
Oxidant-induced activation of cGMP-dependent protein kinase Iα mediates neuropathic pain after peripheral nerve injury.
Article in Antioxidants & redox signaling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Redox-dependent activation of protein kinase G1α contributes to transient receptor potential cation channel subfamily V member 1-mediated acute nociceptive pain behavior.Redox report : communications in free radical research · 2025Article
- Enhancing peripheral nerve regeneration with rehabilitation and biomaterial-driven drug delivery strategies.Progress in biomedical engineering (Bristol, England) · 2025Review
- Nitroxidative Stress, Cell-Signaling Pathways, and Manganese Porphyrins: Therapeutic Potential in Neuropathic Pain.International journal of molecular sciences · 2025Review
- Targeting the nitric oxide/cGMP signaling pathway to treat chronic pain.Neural regeneration research · 2023Review
- NADPH Oxidases in Pain Processing.Antioxidants (Basel, Switzerland) · 2022Review
- The activity of cGMP-dependent protein kinase Iα is not directly regulated by oxidation-induced disulfide formation at cysteine 43.The Journal of biological chemistry · 2017Article
- Redox-guided axonal regrowth requires cyclic GMP dependent protein kinase 1: Implication for neuropathic pain.Redox biology · 2017Article
- Nitroxidative Signaling Mechanisms in Pathological Pain.Trends in neurosciences · 2016Review
- Nuclear Factor-kappaB-Dependent Sestrin2 Induction Mediates the Antioxidant Effects of BDNF Against Mitochondrial Inhibition in Rat Cortical Neurons.Molecular neurobiology · 2016Article
- Structures of cGMP-Dependent Protein Kinase (PKG) Iα Leucine Zippers Reveal an Interchain Disulfide Bond Important for Dimer Stability.Biochemistry · 2015Article
- Cyclic nucleotide signaling in sensory neuron hyperexcitability and chronic pain after nerve injury.Neurobiology of pain (Cambridge, Mass.)Review
- Two isoforms of cyclic GMP-dependent kinase-I exhibit distinct expression patterns in the adult mouse dorsal root ganglion.Molecular painArticle
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
aimsEmerging lines of evidence indicate that oxidants such as hydrogen peroxide exert specific signaling functions during the processing of chronic pain. However, the mechanisms by which oxidants regulate pain processing in vivo remain poorly understood. Here, we investigated whether cyclic guanosine monophosphate (cGMP)-dependent protein kinase Iα (cGKIα), which can be activated by oxidants independently of cGMP, serves as a primary redox target during pain processing.
resultsAfter peripheral nerve injury, oxidant-induced cGKIα activation is increased in dorsal root ganglia of mice. Knock-in (KI) mice in which cGKIα cannot transduce oxidant signals demonstrated reduced neuropathic pain behaviors after peripheral nerve injury, and reduced pain behaviors after intrathecal delivery of oxidants. In contrast, acute nociceptive, inflammatory, and cGMP-induced pain behaviors were not impaired in these mice. INNOVATION: Studying cGKIα KI mice, we provide the first evidence that oxidants activate cGKIα in sensory neurons after peripheral nerve injury in vivo.
conclusionOur results suggest that oxidant-induced activation of cGKIα specifically contributes to neuropathic pain processing, and that prevention of cGKIα redox activation could be a potential novel strategy to manage neuropathic pain.
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