ArticleAntioxidants & redox signaling2013
Antioxidant activity of sestrin 2 controls neuropathic pain after peripheral nerve injury.
Article in Antioxidants & redox signaling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 64 citations in OpenAlex.
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- c-Jun inhibition mitigates chemotherapy-induced neurotoxicity in iPSC-derived sensory neurons.Cell death discovery · 2025Article
- Enhancing peripheral nerve regeneration with rehabilitation and biomaterial-driven drug delivery strategies.Progress in biomedical engineering (Bristol, England) · 2025Review
- Transcriptomic profiling of sciatic nerves and dorsal root ganglia reveals site-specific effects of prediabetic neuropathy.Translational research : the journal of laboratory and clinical medicine · 2024Article
- Role of Oxygen and Its Radicals in Peripheral Nerve Regeneration: From Hypoxia to Physoxia to Hyperoxia.International journal of molecular sciences · 2024Review
- Involvement of Oxidative Stress and Nutrition in the Anatomy of Orofacial Pain.International journal of molecular sciences · 2023Review
- Nox, Nox, Are You There? The Role of NADPH Oxidases in the Peripheral Nervous System.Antioxidants & redox signaling · 2022Review
- NADPH Oxidases in Pain Processing.Antioxidants (Basel, Switzerland) · 2022Review
- Sestrin2 in cancer: a foe or a friend?Biomarker research · 2022Review
- Possible roles of sestrin2 in multiple sclerosis and its relationships with clinical outcomes.Arquivos de neuro-psiquiatria · 2022Article
- The functions and roles of sestrins in regulating human diseases.Cellular & molecular biology letters · 2022Review
- Sestrin2 in hypoxia and hypoxia-related diseases.Redox report : communications in free radical research · 2021Review
- Role of Oxidative DNA Damage and Repair in Atrial Fibrillation and Ischemic Heart Disease.International journal of molecular sciences · 2021Review
- Article
- Knockout of AMPKα2 Blocked the Protection of Sestrin2 Overexpression Against Cardiac Hypertrophy Induced by Pressure Overload.Frontiers in pharmacology · 2021Article
- Implication of sestrin3 in epilepsy and its comorbidities.Brain communications · 2021Article
- Review
- Dexmedetomidine Relieves Neuropathic Pain in Rats With Chronic Constriction Injury via the Keap1-Nrf2 Pathway.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsNeuropathic pain is a chronic debilitating disease that is often unresponsive to currently available treatments. Emerging lines of evidence indicate that reactive oxygen species (ROS) are required for the development and maintenance of neuropathic pain. However, little is known about endogenous mechanisms that neutralize the pain-relevant effects of ROS. In the present study, we tested whether the stress-responsive antioxidant protein Sestrin 2 (Sesn2) blocks the ROS-induced neuropathic pain processing in vivo.
resultsWe observed that Sesn2 mRNA and protein expression was up-regulated in peripheral nerves after spared nerve injury, a well-characterized model of neuropathic pain. Sesn2 knockout (Sesn2(-/-)) mice exhibited considerably increased late-phase neuropathic pain behavior, while their behavior in acute nociceptive and in inflammatory pain models remained unaffected. The exacerbated neuropathic pain behavior of Sesn2(-/-) mice was associated with elevated ROS levels and an enhanced activating transcription factor 3 up-regulation in sensory neurons, and it was reversed by the ROS scavenger N-tert-Butyl-α-phenylnitrone. In contrast, administration of the ROS donor tert-butyl hydroperoxide induced a prolonged pain behavior in naive Sesn2(-/-) mice. INNOVATION: We show that the antioxidant function of Sesn2 limits neuropathic pain processing in vivo.
conclusionSesn2 controls ROS-dependent neuropathic pain signaling after peripheral nerve injury and may, thus, provide a potential new target for the clinical management of chronic neuropathic pain conditions.
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