ArticleFrontiers in molecular neuroscience2022
Mitochondrial Reactive Oxygen Species Mediate Activation of TRPV1 and Calcium Entry Following Peripheral Sensory Axotomy.
Article in Frontiers in molecular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 12 citations in OpenAlex.
- Aging-Related Changes in the Injury Response of the Peripheral Nervous System.Neuroscience bulletin · 2026Review
- Mitochondrial dysfunction at the intersection of alcohol use disorder and chronic pain.Function (Oxford, England) · 2026Review
- Nanomolar Cadmium Disrupts Neurotransmitter Release Timing via a ROS-dependent Mechanism at the Mouse Neuromuscular Junction: Modulation by Nanomolar ZnNeurochemical research · 2026Article
- Mitochondrial dysfunction in the spinal cord contributes to peripheral hypersensitivity in a nitroglycerin-induced migraine model.Journal of translational medicine · 2026Article
- Pathological Interplay of ROS With Myofibroblasts: An Impediment to Corneal Restitution.Oxidative medicine and cellular longevity · 2026Review
- The short-term and long-term effect of burn on organ dysfunction: mechanisms and strategies.Frontiers in immunology · 2026Review
- The interaction between oxidative stress and Schwann cells.Experimental biology and medicine (Maywood, N.J.) · 2026Review
- 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
- TRPV1 channel antagonist capsazepine alleviates morphine tolerance and morphine-induced neurotoxicity by preventing mitochondrial damage and apoptosis: an in vivo and in vitro study.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Local production of reactive oxygen species drives vincristine-induced axon degeneration.Cell death & disease · 2023Article
- NADAntioxidants & redox signaling · 2023Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Axons that are physically separated from their soma activate a series of signaling events that results in axonal self-destruction. A critical element of this signaling pathway is an intra-axonal calcium rise that occurs just prior to axonal fragmentation. Previous studies have shown that preventing this calcium rise delays the onset of axon fragmentation, yet the ion channels responsible for the influx, and the mechanisms by which they are activated, are largely unknown. Axonal injury can be modeled
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What OpenQuestion holds
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.