ArticleScience advances2022
Follistatin promotes LIN28B-mediated supporting cell reprogramming and hair cell regeneration in the murine cochlea.
Article in Science advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 46 citations in OpenAlex.
- Engineering exosomes in the treatment of sensorineural hearing loss: from basic research to clinical applications.Frontiers in molecular neuroscience · 2026Review
- Inner ear organoids: Recent progress and potential applications.Fundamental research · 2025Review
- Implication of GPRASP2 in the Proliferation and Hair Cell-Forming of Cochlear Supporting Cells.Cell proliferation · 2025Article
- The RNA-binding protein TRIM71 is essential for hearing in humans and mice and times auditory sensory organ development.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The Notch ligand Jagged1 plays a dual role in cochlear hair cell regeneration.Nature communications · 2025Article
- AAV-Sparcl1 promotes hair cell regeneration by increasing supporting cell plasticity.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Conditional Overexpression of Serpine2 Promotes Hair Cell Regeneration from Lgr5+ Progenitors in the Neonatal Mouse Cochlea.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Conditional Overexpression of Net1 Enhances the Trans-Differentiation of Lgr5Cell proliferation · 2025Article
- An atlas of neuropathic pain-associated molecular pathological characteristics in the mouse spinal cord.Communications biology · 2025Article
- Review
- Roles of supporting cells in the maintenance and regeneration of the damaged inner ear: A literature review.Journal of otology · 2024Review
- Metabolic Profiling of Cochlear Organoids Identifies α-Ketoglutarate and NADAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Pcolce2 overexpression promotes supporting cell reprogramming in the neonatal mouse cochlea.Cell proliferation · 2024Article
- MEK/ERK signaling drives the transdifferentiation of supporting cells into functional hair cells by modulating the Notch pathway.Stem cells translational medicine · 2024Article
- Molecular Specializations Underlying Phenotypic Differences in Inner Ear Hair Cells of Zebrafish and Mice.bioRxiv : the preprint server for biology · 2024Article
- The Reign of Follistatin in Tumors and Their Microenvironment: Implications for Drug Resistance.Biology · 2024Review
- Extracellular vesicles for developing targeted hearing loss therapy.Journal of controlled release : official journal of the Controlled Release Society · 2024Review
- Hair Cell Regeneration: From Animals to Humans.Clinical and experimental otorhinolaryngology · 2024Review
- An essential signaling cascade for avian auditory hair cell regeneration.Developmental cell · 2024Article
- GelMA/PEDOT:PSS Composite Conductive Hydrogel-Based Generation and Protection of Cochlear Hair Cells through Multiple Signaling Pathways.Biomolecules · 2024Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Hair cell (HC) loss within the inner ear cochlea is a leading cause for deafness in humans. Before the onset of hearing, immature supporting cells (SCs) in neonatal mice have some limited capacity for HC regeneration. Here, we show that in organoid culture, transient activation of the progenitor-specific RNA binding protein LIN28B and Activin antagonist follistatin (FST) enhances regenerative competence of maturing/mature cochlear SCs by reprogramming them into progenitor-like cells. Transcriptome profiling and mechanistic studies reveal that LIN28B drives SC reprogramming, while FST is required to counterbalance hyperactivation of transforming growth factor-β-type signaling by LIN28B. Last, we show that LIN28B and FST coactivation enhances spontaneous cochlear HC regeneration in neonatal mice and that LIN28B may be part of an endogenous repair mechanism that primes SCs for HC regeneration. These findings indicate that SC dedifferentiation is critical for HC regeneration and identify LIN28B and FST as main regulators.
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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 OpenQuestion graph.