ArticleFrontiers in cellular neuroscience2018
Spontaneous Hair Cell Regeneration Is Prevented by Increased Notch Signaling in Supporting Cells.
Article in Frontiers in cellular neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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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
23 citing papers in PubMed, 34 citations in OpenAlex.
- The aryl hydrocarbon receptor is expressed in non-sensory cells in the cochlea and regulates hair cell survival.Frontiers in molecular neuroscience · 2026Article
- The Notch ligand Jagged1 plays a dual role in cochlear hair cell regeneration.Nature communications · 2025Article
- Kolliker's Organ and Its Functional Role in the Development of Corti's Organ and Auditory Systems.Audiology research · 2025Review
- Sponge bHLH Gene Expression inInternational journal of molecular sciences · 2025Article
- Hearing restoration through hair cell regeneration: A review of recent advancements and current limitations.Hearing research · 2025Review
- Reprogramming withPNAS nexus · 2024Article
- Hair Cell Regeneration: From Animals to Humans.Clinical and experimental otorhinolaryngology · 2024Review
- The transcription factorFrontiers in cellular neuroscience · 2024Article
- SoxC transcription factors shape the epigenetic landscape to establish competence for sensory differentiation in the mammalian organ of Corti.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- On the value of diverse organisms in auditory research: From fish to flies to humans.Hearing research · 2023Review
- Editorial: New insights in molecular pathways in ototoxicity.Frontiers in cellular neuroscience · 2023Article
- Uncovering Novel Prognostic Factors of Sudden Sensorineural Hearing Loss by Whole-Genome Sequencing of Cell-Free DNA.The journal of international advanced otology · 2022Article
- The regenerative capacity of neonatal tissues.Development (Cambridge, England) · 2022Review
- In vitro and in vivo models: What have we learnt about inner ear regeneration and treatment for hearing loss?Molecular and cellular neurosciences · 2022Review
- Follistatin promotes LIN28B-mediated supporting cell reprogramming and hair cell regeneration in the murine cochlea.Science advances · 2022Article
- Kölliker's organ-supporting cells and cochlear auditory development.Frontiers in molecular neuroscience · 2022Review
- Molecular Pathways Modulating Sensory Hair Cell Regeneration in Adult Mammalian Cochleae: Progress and Perspectives.International journal of molecular sciences · 2021Review
- The interaction of Notch and Wnt signaling pathways in vertebrate regeneration.Cell regeneration (London, England) · 2021Review
- Perspectives on Human Hearing Loss, Cochlear Regeneration, and the Potential for Hearing Restoration Therapies.Brain sciences · 2020Review
- Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
During embryonic development, differentiation of cochlear progenitor cells into hair cells (HCs) or supporting cells (SCs) is partially controlled through Notch signaling. Many studies have shown that inhibition of Notch signaling allows SCs to convert into HCs in both normal and drug damaged neonatal mouse cochleae. This mechanism is also implicated during HC regeneration in non-mammalian vertebrates; however, the mechanism of spontaneous HC regeneration in the neonatal mouse cochlea is less understood. While inhibition of Notch signaling can force SCs to convert into HCs and increase the number of regenerated HCs, it is currently unknown whether this pathway is involved in spontaneous HC regeneration observed
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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.