ArticleToxicology research2025
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.
Article in Toxicology research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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
Cisplatin causes hearing loss in at least 60% of chemotherapy patients, leading to impairments in the patient's life quality. Spiral ganglion neurons (SGNs) and hair cells (HCs) are the main cell types affected by cisplatin accumulation in the inner ear. Fasudil is an FDA-approved drug and has been reported to exert neuroprotective effects in previous research. However, whether fasudil possesses protective effects in cisplatin-induced SGN and HC damage and the potential mechanisms remain unknown. In this study, we investigated whether fasudil has a protective effect on cisplatin-induced damage to inner ear SGNs and HCs. We first observed the effect of different concentrations of fasudil on cisplatin-induced cell loss of SGNs and HCs. We also studied the effects of fasudil on cisplatin-induced apoptosis of SGNs and HCs and detected the mitochondrial reactive oxygen species (ROS) level. Furthermore, we investigated the mechanisms of fasudil in protecting the SGNs and HCs from cisplatin- induced cells apoptosis. We found that fasudil treatment significantly ameliorated SGNs and HCs loss and attenuated cell apoptosis after cisplatin exposure. Moreover, fasudil attenuated the cisplatin-induced ROS generation in SGN- and HC-explants culture. Further mechanistic studies revealed that fasudil regulated the ROCK/PTEN/AKT signaling pathway in SGN- and HC-explants after cisplatin exposure. This study indicates that fasudil might be a novel therapeutic target for preventing cisplatin-induced SGNs and HCs damage.
Indexed as
Identifiers
What Socratic 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 Socratic graph.