ReviewFrontiers in molecular biosciences2025
The role of antioxidants in facial nerve injury.
Review in Frontiers in molecular biosciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Evaluation of Dexamethasone and Swimming Exercise as Complementary Interventions in a Rat Sciatic Nerve Injury Model.Antioxidants (Basel, Switzerland) · 2025Article
- The interaction of regulated forms of cell death in the pathogenesis of severe facial paralysis and potential therapeutic strategies.Frontiers in neuroscience · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative stress contributes to the pathogenesis of facial nerve injury (FNI), yet the role of antioxidants in driving regeneration and functional recovery remains incompletely defined. This narrative review synthesizes studies published between 2008 and 2025 that evaluated antioxidant interventions in FNI across animal and limited human contexts. We systematically searched five databases and included 19 studies assessing oxidative stress markers and neural outcomes following antioxidant administration. To avoid overgeneralization, we stratified findings by injury model-crush/compression, transection with anastomosis, and ischemic/viral-and by primary endpoints (electrophysiology/behavior vs. histology/biochemistry), and, where reported, by intervention timing and dose. Antioxidants commonly reduced reactive oxygen species and modulated survival and inflammatory pathways, supporting neuroprotection and, in some models, improved electrophysiological or behavioral readouts. However, benefits varied by model and regimen: crush injuries showed earlier functional gains, whereas transection models more often demonstrated histological improvement without consistent short-term functional recovery; ischemic/viral studies frequently lacked standardized electrophysiological confirmation. Outcomes were also contingent on timing and dose (with earlier initiation and moderate dosing generally more favorable), and select combinations showed additive effects in preclinical settings. Overall, the evidence is predominantly preclinical, heterogeneous in dosing/timing/formulations, and limited by small sample sizes and inconsistent functional outcomes. Antioxidant strategies should therefore be considered hypothesis-generating rather than clinically recommendable at this time. Future research should use model-appropriate, standardized functional endpoints, prespecify timing/dose exploration, evaluate rational combinations, and conduct well-powered clinical trials to establish efficacy, optimal use, and safety.
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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.