ArticleMolecules and cells2025
Biallelic variants of SEMA3F are associated with nonsyndromic hearing loss.
Article in Molecules and cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Molecules and Cells 2025, highlights from molecules to organisms.Molecules and cells · 2026Article
- HAP1 interaction with KCNQ4 attenuates channel surface expression and function.Molecules and cells · 2026Article
- Cryopreserved Human Otic Neuronal Spheroids Self-assemble for Functional Connectivity Analysis and Long-term Ototoxicity Evaluation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Auditory genotype-phenotype correlation of patients with variants in STRC.Scientific reports · 2025Article
- Recent preclinical and clinical advances in gene therapy for hereditary hearing loss.Molecules and cells · 2025Review
- TMEM145 is a key stereociliary component in the link structures of outer hair cells and mediates the secretion of stereocilin and tubby.Nature communications · 2025Article
- Leveraging underrepresented population data improves interpretation of genetic variants associated with hearing loss.Scientific reports · 2025Article
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Authors and funding
12 authors.
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Abstract
It is crucial to manage hearing loss and its associated public health impacts. In this study, we aimed to understand the role of Sema3f in the development and maintenance of the auditory system. Inner ear-specific Sema3f knockout mice exhibited hearing loss at 8 weeks with an elevated threshold for auditory brainstem response and an absent threshold for distortion product optoacoustic emission tests. Additionally, an increased number of outer hair cells and abnormal patterns of spiral ganglion neuron projections in the outer hair cell regions were observed. Through the analyses of sequencing data from 558 families with hearing loss, we identified biallelic variants of SEMA3F, which encodes semaphorin-3F, in one of the families. In the family, the proband showed profound progressive nonsyndromic hearing loss with congenital onset. In vitro analysis revealed that the identified missense variants decreased the furin-mediated processing of SEMA3F and abolished the cellular abilities of SEMA3F, which collapsed the filamentous actin cytoskeleton in human umbilical vein-derived endothelial cells. Our data suggest that SEMA3F is essential for normal hearing and is associated with nonsyndromic hearing loss in humans.
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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.