Following severe injury, most cells in the vestibular sensory epithelium undergo cell death, whereas the surviving epithelial cells initiate a repair program that leads to the formation of a flat epithelium (FE). However, the mechanisms underlying FE formation remain unclear. In this study, we combine in vivo and in vitro approaches to investigate the role of TGF-β signaling in this process....
No actionable change for clinical practice; this is early-stage basic science in a mouse model that may one day inform vestibular regeneration therapies.
Understanding how scar tissue forms in the injured inner ear balance organ is a key barrier to developing regenerative treatments for vestibular disorders.
- 01TGF-β signaling promotes flat epithelium (scar-like layer) formation in the injured mouse utricle.
- 02The mechanism involves epithelial-mesenchymal transition (cells shifting from sensory to scar-forming type) in surviving cells.
- 03Severe injury model was used, relevant to understanding worst-case inner ear damage scenarios.
- 04Findings are limited to adult mouse utricle; human translation is unknown.
- 05Published in Hearing Research (DOI: 10.1016/j.heares.2026.109727).
TGF-β signaling drives flat epithelium formation in the severely injured adult mouse utricle via epithelial-mesenchymal transition.
studysupportedEpithelial-mesenchymal transition in surviving cells contributes to failed regeneration after vestibular injury.
studypartially supported- PMID
- 42398320
- DOI
- 10.1016/j.heares.2026.109727.
- Journal
- Hearing Research
- Publication type
- research_article
- Evidence level
- 4
- Population
- Adult mice with severely injured utricle (vestibular organ)
- Intervention
- Severe vestibular injury with observation of TGF-β signaling and epithelial-mesenchymal transition
Primary outcomes
Flat epithelium formation in injured utricle; Role of TGF-β signaling in epithelial-mesenchymal transition