ArticleNature aging2025
mRNA metabolism regulator human antigen R (HuR) regulates age-related hearing loss in aged mice.
Article in Nature aging, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 6 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.
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Who cites it
6 citing papers in PubMed.
- HuR modulates disease-relevant alternative splicing of MAPT and other Alzheimer's disease-related genes.Molecular genetics and genomics : MGG · 2026Article
- Transcriptomics Implicates the G3BP1-SG Axis in Cochlear Hair-Cell Pyroptosis During Age-Related Hearing Loss.Journal of cellular and molecular medicine · 2026Article
- Dietary Zinc Glycine Supplementation Attenuates Aging-Driven Cochlear Hair Cell Oxidative Injury and Hearing Loss.Nutrients · 2026Article
- Article
- RNA-binding proteins in aging and age-related diseases: roles, mechanisms, and a large language model analysis.Biogerontology · 2026Review
- Advances in the treatment of age-related hearing loss: from molecular mechanisms to targeted interventions.Frontiers in aging neuroscience · 2026Review
Corrections and comments
- Erratum issued
Authors and funding
20 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Age-related hearing loss (ARHL) is among the most prevalent and complex disorders in older adults. However, the pathogenesis of ARHL remains poorly understood. Using a single-cell transcriptomic landscape of mouse cochlea at five time points (1, 2, 5, 12 and 15 months), we found that the levels of human antigen R (HuR)-a classical RNA-binding protein-increase with age. Here we show that HuR is specifically transported from the nucleus to the cytoplasm in hair cells in both aging mice and nonhuman primates. HuR overexpression in cochlea could successfully alleviate ARHL in aged mice. Meanwhile, HuR deficiency led to premature hearing dysfunction characterized by degeneration of stereocilia and the subsequent loss of hair cells. RNA immunoprecipitation sequencing analysis revealed that HuR can bind to messenger RNAs that enable stereocilia maintenance, including Gnai3. Adeno-associated virus-mediated Gnai3 overexpression partially rescues the hearing defects in HuR-deficient mice. Taken together, these findings indicate that HuR is a potential therapeutic target for ARHL.
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Registered trials
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