ArticleThe Laryngoscope2017
SMAD3 expression and regulation of fibroplasia in vocal fold injury.
Article in The Laryngoscope, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Redox-regulated in situ-forming hydrogel informed by single-cell transcriptomics for functional restoration of injured vocal folds.Nature communications · 2026Article
- Regenerative Strategies for Vocal Fold Repair Using Injectable Materials.Biomimetics (Basel, Switzerland) · 2025Review
- Preclinical Vocal Fold and Airway Injury Models: A Scoping Review.Laryngoscope investigative otolaryngology · 2025Review
- SOCS3 Silencing Promotes Activation of Vocal Fold Fibroblasts via JAK2/STAT3 Signaling Pathway.Inflammation · 2023Article
- A xenograft study of human adipose stromal cell-based vocal fold mucosal replacement in rabbits.Laryngoscope investigative otolaryngology · 2022Article
- Concurrent YAP/TAZ and SMAD signaling mediate vocal fold fibrosis.Scientific reports · 2021Article
- Article
- Quantifying vocal fold wound-healing biomechanical property changes.The Laryngoscope · 2020Article
- Implementing Efficient Peptoid-Mediated Delivery of RNA-Based Therapeutics to the Vocal Folds.Laryngoscope investigative otolaryngology · 2019Article
- The effects of cytosporone-B, a novel antifibrotic agent, on vocal fold fibroblasts.The Laryngoscope · 2018Article
- Nanoparticle delivery of RNA-based therapeutics to alter the vocal fold tissue response to injury.The Laryngoscope · 2018Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
objectiveRecent reports highlight the efficacy of small interfering RNA (siRNA) targeting SMAD3 to regulate transforming growth factor β (TGF-β)-mediated fibroplasia in vocal fold fibroblasts. The current study sought to investigate SMAD3 expression during wound healing in vivo and quantify the downstream transcriptional events associated with SMAD3 knockdown in vitro. STUDY
designIn vivo and in vitro.
methodsUnilateral vocal fold injury was created in a rabbit model. SMAD3 and SMAD7 mRNA expression was quantified at 1 hour and 1, 3, 7, 14, 30, 60, and 90 days following injury. In vitro, multi-gene analysis technology was employed in our immortalized human vocal-fold fibroblast cell line following TGF-β1 stimulation ± SMAD3 knockdown across time points.
resultsSMAD3 mRNA expression increased following injury; upregulation was significant at 3 and 7 days compared to control (both P < 0.001). SMAD7 mRNA was also upregulated at 3, 7, and 14 days (P = 0.02, P < 0.001, and P < 0.001, respectively). In vitro, SMAD3 knockdown reduced the expression of multiple profibrotic, TGF-β signaling, and extracellular matrix metabolism genes at 6 and 24 hours following TGF-β1 stimulation.
conclusionCumulatively, these data support SMAD3 as a potential master regulator of TGF-β-mediated fibrosis. SMAD3 transcription peaked 7 days following injury. Multi-gene analysis indicated that the therapeutic effectiveness of SMAD3 knockdown may be related to regulation of downstream mediators of fibroplasia and altered TGF-β signaling. LEVEL OF EVIDENCE: NA. Laryngoscope, 127:E308-E316, 2017.
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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.