ArticleAging cell2023
Releasing YAP dysfunction-caused replicative toxicity rejuvenates mesenchymal stem cells.
Article in Aging cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- SenFlag gene signature identifies senescent cells in mouse and human tissues through a conserved core transcriptional program.The EMBO journal · 2026Article
- NFATC1 dysfunction-triggered MSC senescence induces tooth aging amenable to senolytic therapy.Stem cell reports · 2026Article
- Research progress on cellular senescence in the pathogenesis and treatment of osteoarthritis and temporomandibular joint osteoarthritis.Journal of oral & facial pain and headache · 2026Review
- Magnesium-doped bioactive glass enhances bone regeneration by reversing replicative senescence of human dental pulp stem cells in bone defect therapy.Regenerative biomaterials · 2026Article
- Multi-omics approach reveals TGF-β signaling-driven senescence in periodontium stem cells.Journal of advanced research · 2025Article
- Releasing YAP dysfunction-caused replicative toxicity rejuvenates mesenchymal stem cells.Aging cell · 2023Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hippo-independent YAP dysfunction has been demonstrated to cause chronological aging of stromal cells by impairing the integrity of nuclear envelope (NE). In parallel with this report, we uncover that YAP activity also controls another type of cellular senescence, the replicative senescence in in vitro expansion of mesenchymal stromal cells (MSCs), but this event is Hippo phosphorylation-dependent, and there exist another NE integrity-independent downstream mechanisms of YAP. Specifically, Hippo phosphorylation causes reduced nuclear/active YAP and then decreases the level of YAP protein in the proceeding of replicative senescence. YAP/TEAD governs RRM2 expression to release replicative toxicity (RT) via licensing G1/S transition. Besides, YAP controls the core transcriptomics of RT to delay the onset of genome instability and enhances DNA damage response/repair. Hippo-off mutations of YAP (YAP
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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 Socratic graph.