ArticleFrontiers in physiology2018
TNF-α Increases Production of Reactive Oxygen Species through Cdk5 Activation in Nociceptive Neurons.
Article in Frontiers in physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.
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- Targeting the Main Sources of Reactive Oxygen Species Production: Possible Therapeutic Implications in Chronic Pain.Current neuropharmacology · 2024Review
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- Oxidative stress in the brain and retina after traumatic injury.Frontiers in neuroscience · 2023Review
- Potential Therapeutic Approach of Melatonin against Omicron and Some Other Variants of SARS-CoV-2.Molecules (Basel, Switzerland) · 2022Review
- NADPH Oxidases in Pain Processing.Antioxidants (Basel, Switzerland) · 2022Review
- Apoptosis and (in) Pain-Potential Clinical Implications.Biomedicines · 2022Review
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Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The participation of reactive oxygen species (ROS) generated by NOX1 and NOX2/NADPH oxidase has been documented during inflammatory pain. However, the molecular mechanism involved in their activation is not fully understood. We reported earlier a key role of Cyclin-dependent kinase 5 (Cdk5) during inflammatory pain. In particular, we demonstrated that TNF-α increased p35 expression, a Cdk5 activator, causing Cdk5-mediated TRPV1 phosphorylation followed by an increment in Ca
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.