ArticleFrontiers in cellular neuroscience2014
In vivo overexpression of X-linked inhibitor of apoptosis protein protects against neomycin-induced hair cell loss in the apical turn of the cochlea during the ototoxic-sensitive period.
Article in Frontiers in cellular neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 54 citations in OpenAlex.
- NOX2 Contributes to High-Frequency Outer Hair Cell Vulnerability in the Cochlea.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Lycium barbarum Glycopeptide Alleviates Neomycin-Induced Ototoxicity by Inhibiting Tryptophan Hydroxylase-Mediated Serotonin Biosynthesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Protective Effect of Avenanthramide-C on Auditory Hair Cells against Oxidative Stress, Inflammatory Cytokines, and DNA Damage in Cisplatin-Induced Ototoxicity.International journal of molecular sciences · 2023Article
- Mechanisms and otoprotective strategies of programmed cell death on aminoglycoside-induced ototoxicity.Frontiers in cell and developmental biology · 2023Review
- Apoptosis and tissue thinning contribute to symmetric cell division in the developing mouse epidermis in a nonautonomous way.PLoS biology · 2022Article
- Specific knockdown ofMolecular therapy. Nucleic acids · 2022Article
- Mild Therapeutic Hypothermia and Putative Mechanisms of Hair Cell Survival in the Cochlea.Antioxidants & redox signaling · 2022Article
- Sox2 overexpression alleviates noise-induced hearing loss by inhibiting inflammation-related hair cell apoptosis.Journal of neuroinflammation · 2022Article
- Hippo/YAP signaling pathway protects against neomycin-induced hair cell damage in the mouse cochlea.Cellular and molecular life sciences : CMLS · 2022Article
- Novel m.4268T>C mutation in the mitochondrial tRNAWorld journal of clinical cases · 2022Article
- Multiple Sevoflurane Exposures During the Neonatal Period Cause Hearing Impairment and Loss of Hair Cell Ribbon Synapses in Adult Mice.Frontiers in neuroscience · 2022Article
- FGF22 deletion causes hidden hearing loss by affecting the function of inner hair cell ribbon synapses.Frontiers in molecular neuroscience · 2022Article
- Prevention of acquired sensorineural hearing loss in mice by in vivo Htra2 gene editing.Genome biology · 2021Article
- Autophagy impairment as a key feature for acetaminophen-induced ototoxicity.Cell death & disease · 2021Article
- Autophagy: A Novel Horizon for Hair Cell Protection.Neural plasticity · 2021Review
- Molecular Behavior of HMGB1 in the Cochlea Following Noise Exposure andFrontiers in cell and developmental biology · 2021Article
- Low-Intensity Ultrasound Causes Direct Excitation of Auditory Cortical Neurons.Neural plasticity · 2021Article
- Deletion of Clusterin Protects Cochlear Hair Cells against Hair Cell Aging and Ototoxicity.Neural plasticity · 2021Article
- Key Signaling Pathways Regulate the Development and Survival of Auditory Hair Cells.Neural plasticity · 2021Review
- Dose-Dependent Pattern of Cochlear Synaptic Degeneration in C57BL/6J Mice Induced by Repeated Noise Exposure.Neural plasticity · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aminoglycoside-induced cochlear ototoxicity causes hair cell (HC) loss and results in hearing impairment in patients. Previous studies have developed the concept of an ototoxicity-sensitive period during which the cochleae of young mice are more vulnerable to auditory trauma than adults. Here, we compared neomycin-induced ototoxicity at the following four developmental ages in mice: postnatal day (P)1-P7, P8-P14, P15-P21, and P60-P66. We found that when neomycin was administered between P8 and P14, the auditory brainstem response threshold increase was significantly higher at low frequencies and HC loss was significantly greater in the apical turn of the cochlea compared to neomycin administration during the other age ranges. Quantitative real-time PCR (qPCR) data revealed that the expression of apoptotic markers, including Casp3 and Casp9, was significantly higher when neomycin was injected from P8 to P14, while the expression of the X-linked inhibitor of apoptosis protein (XIAP) gene was significantly higher when neomycin was injected from P60 to P66. Because XIAP expression was low during the neomycin-sensitive period, we overexpressed XIAP in mice and found that it could protect against neomycin-induced hearing loss at low frequencies and HC loss in the apical turn of the cochlea. Altogether, our findings demonstrate a protective role for XIAP against neomycin-induced hearing loss and HC loss in the apical turn of the cochlea during the ototoxic-sensitive period, and suggest that apoptotic factors mediate the effect of neomycin during the ototoxic-sensitive period.
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.