ArticleStem cell reports2022
YAP signaling in horizontal basal cells promotes the regeneration of olfactory epithelium after injury.
Article in Stem cell reports, 2022. 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, 12 citations in OpenAlex.
- Olfactory epithelium regeneration and homeostasis: cellular and molecular mechanisms and novel methodological advances.Cell regeneration (London, England) · 2026Review
- Asymmetric histone inheritance regulates olfactory stem cell fates during regeneration.Nature communications · 2026Article
- Mechanical constraints on cell plasticity: insights from the olfactory epithelium.Frontiers in cell and developmental biology · 2026Review
- Stem Cell Niches for Olfactory Regeneration and Their Therapeutic Applications.Journal of rhinology : official journal of the Korean Rhinologic Society · 2025Review
- Differential efficacy of olfactory neurospheres from deviated nasal septum and chronic rhinosinusitis patients in regenerating olfactory epithelium.Stem cell research & therapy · 2025Article
- Olfactory dysfunction and the role of stem cells in the regeneration of olfactory neurons.Heliyon · 2024Review
- Horizontal basal cells self-govern their neurogenic potential during injury-induced regeneration of the olfactory epithelium.Development (Cambridge, England) · 2023Article
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Authors and funding
21 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The horizontal basal cells (HBCs) of olfactory epithelium (OE) serve as reservoirs for stem cells during OE regeneration, through proliferation and differentiation, which is important in recovery of olfactory function. However, the molecular mechanism of regulation of HBC proliferation and differentiation after injury remains unclear. Here, we found that yes-associated protein (YAP) was upregulated and activated in HBCs after OE injury. Deletion of YAP in HBCs led to impairment in OE regeneration and functional recovery of olfaction after injury. Mechanically, YAP was activated by S1P/S1PR2 signaling, thereby promoting the proliferation of HBCs and OE regeneration after injury. Finally, activation of YAP signaling enhanced the proliferation of HBCs and improved functional recovery of olfaction after OE injury or in Alzheimer's disease model mice. Taken together, these results reveal an S1P/S1PR2/YAP pathway in OE regeneration in response to injury, providing a promising therapeutic strategy for OE injury.
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