ArticleJournal of neurochemistry2025
BH4 Oxidation-Derived H
Article in Journal of neurochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- BH4 Oxidation-Derived HJournal of neurochemistry · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Elevated Tetrahydrobiopterin (BH4) levels are linked to various pain conditions. Pharmacological or genetic reduction of BH4 levels has analgesic effects in rodent models of neuropathic and inflammatory pain, but also affects neurological and cardiovascular functions. Little is known about the downstream mechanisms of BH4 that could be targeted to attenuate BH4-induced pain hypersensitivity without lowering BH4 levels. In this study, we exposed ex vivo-cultured rat dorsal root ganglion (DRG) neurons to BH4 and analyzed the activity of the sensory neuron-sensitizing kinase ERK1/2 via high-content imaging. We show that BH4 exposure leads to increased pERK1/2 levels in a dose- and time-dependent manner. Interestingly, we found that H
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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.