ArticleScientific reports2025
In vitro evaluation of Verteporfin and exploration of TEAD palmitoylation inhibition in Piezo1-YAP/TAZ signaling and ECM remodeling.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The trial behind it
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
10 citing papers in PubMed.
- Screening of peptide inhibitors targeting YAP-TEAD4 interaction: affinity evaluation and anti-AML cell activity.Journal of enzyme inhibition and medicinal chemistry · 2026Article
- Hippo Pathway-YAP/TAZ Signaling: Molecular Mechanisms, Biological Function, Diseases, and Therapeutic Targets.MedComm · 2026Review
- Targeting AMPK signaling in nucleus pulposus cells ameliorates spaceflight microgravity-induced intervertebral disc degeneration.Cell death and differentiation · 2026Article
- Disruption of YAP biomolecular condensates by mechanical stress drives intervertebral disc vascularization.Science advances · 2026Article
- TM4SF1 mediates YAP/TAZ regulation of coronary artery formation.Scientific reports · 2026Article
- Review
- The Stiff Side of Cancer: How Matrix Mechanics Rewrites Non-Coding RNA Expression Programs.Non-coding RNA · 2026Review
- Mechanotransduction in intervertebral disc degeneration: from compartment-specific sensors to translational frontiers.Frontiers in bioengineering and biotechnology · 2026Review
- From mechanotransduction to manual therapy: advances in piezo/TRP channels and lumbar degeneration.Frontiers in physiology · 2026Review
- Luteolin and its derivatives: modulation of epithelial-mesenchymal transition in fibrosis and cancer.Frontiers in pharmacology · 2026Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Fibrosis is characterized by excessive extracellular matrix (ECM) deposition driven by mechanical stress, yet the underlying molecular mechanisms remain incompletely understood. To investigate whether mechanical stress-induced ECM remodeling is mediated by YAP/TAZ-TEAD signaling and whether pharmacological modulation can mimic or reverse these effects. Nucleus pulposus (NP) cells were exposed to mechanical stress and treated with the MST1/2 inhibitor XMU-MP-1 or the YAP/TAZ-TEAD inhibitor Verteporfin (VP). Nuclear localization of YAP/TAZ-TEAD, expression of canonical TEAD target genes (CTGF, CYR61, ANKRD1), and ECM markers (Col1, Col2, α-SMA, FN, CTGF) were analyzed by Western blot, qPCR, and immunofluorescence. Mechanical stress induced nuclear accumulation of YAP/TAZ-TEAD, upregulated TEAD target genes, and promoted profibrotic ECM remodeling. XMU-MP-1 recapitulated these effects, while VP suppressed TEAD-dependent transcription and reversed ECM remodeling without affecting nuclear localization. YAP/TAZ-TEAD signaling mediates mechanically induced ECM remodeling. Activation of this pathway drives profibrotic gene expression, and disruption of YAP-TEAD interaction effectively reverses these changes, highlighting a potential therapeutic target for fibrosis.
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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.