ArticleExperimental and therapeutic medicine2022
Fasudil prevents neomycin-induced hair cell damage by inhibiting autophagy through the miR-489/NDP52 signaling pathway in HEI-OC1 cells.
Article in Experimental and therapeutic medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
8 citing papers in PubMed.
- Targeting Autophagy for Otoprotection: Translating Basic Mechanisms into Clinical Strategies.International journal of molecular sciences · 2026Review
- Autophagy in Sensorineural Hearing Loss: Jekyll or Hyde?International journal of molecular sciences · 2026Review
- Epigenetic Modifications in Sensorineural Hearing Loss: Protective Mechanisms and Therapeutic Potential.Current medical science · 2025Review
- Fasudil protects spiral ganglion neurons and hair cells against cisplatin-induced apoptosis by inhibiting reactive oxygen species accumulation and regulating the ROCK/PTEN/AKT signaling pathway.Toxicology research · 2025Article
- Development of the inner ear and regeneration of hair cells after hearing impairment.Fundamental research · 2025Review
- Beyond the auditory system: cognitive implications of age-related hearing loss.Frontiers in aging neuroscience · 2025Review
- Protective Effects of Fasudil Against Cisplatin-Induced Ototoxicity in Zebrafish: An In Vivo Study.International journal of molecular sciences · 2024Article
- Mitophagy in ototoxicity.Frontiers in cellular neuroscience · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hearing loss is a common sensory disorder that is mainly caused by the loss of hair cells (HCs). Drug-induced deafness, for which there is currently no effective treatment, is mainly caused by the inappropriate use of aminoglycoside antibiotics. Fasudil (Fas), a novel isoquinoline sulfonamide derivative, has exhibited antioxidant abilities in a number of previous studies. The aim of the present study was to investigate the potential effects of Fas against neomycin (Neo)-induced hair cell damage and elucidate the underlying mechanism. Flow cytometry and western blot analysis were used to detect the effects of Fas on cell apoptosis and to determine the expression levels of autophagy-related proteins, LC3B and Beclin 1, induced by Neo. Mitochondrial membrane potential and reactive oxygen species (ROS) levels were detected using fluorescent probes. The effect of Fas on Neo-induced hair cell injury marker, GFP-LC3B, was also examined using the immunofluorescence technique. Fas was found to inhibit Neo-induced mitochondrial autophagy and mitochondrial membrane potential decline, in addition to reducing ROS levels and cell apoptosis caused by Neo treatment. However, Fas failed to inhibit the Neo-induced these above changes in cells with NDP52 overexpression. The putative binding sites of microRNA (miR)-489 on the 3'-untranslated region of nuclear dot protein 52 (NDP52) were predicted using the TargetScan 7.0 online tool, and this association was further verified using a dual-luciferase reporter assay. Moreover, the expression of miR-489 negatively regulated the expression of NDP52. Fas and miR-489 mimic inhibited the Neo-induced mitochondrial autophagy and mitochondrial membrane potential decline, in addition to reducing ROS levels and cell apoptosis. Knockdown of miR-489 expression using a miR-489 inhibitor blocked the inhibitory effects of Fas on the mitochondrial membrane potential, cell apoptosis and ROS production. Therefore, Fas may upregulate the expression of miR-489 to negatively regulate the expression of NDP52 at the post-transcriptional level, which in turn inhibits the activation of mitophagy and cell injury induced by Neo. Thus, Fas may act as a novel therapeutic option in the clinical treatment of hearing loss in the future.
Indexed as
Identifiers
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.