ArticleThe Laryngoscope2017
NR4A1 is an endogenous inhibitor of vocal fold fibrosis.
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 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- Preclinical Vocal Fold and Airway Injury Models: A Scoping Review.Laryngoscope investigative otolaryngology · 2025Review
- SPDEF ameliorates UUO-induced renal fibrosis by transcriptional activation of NR4A1.Molecular medicine (Cambridge, Mass.) · 2024Article
- Article
- A xenograft study of human adipose stromal cell-based vocal fold mucosal replacement in rabbits.Laryngoscope investigative otolaryngology · 2022Article
- NR4A1 inhibits the epithelial-mesenchymal transition of hepatic stellate cells: Involvement of TGF-β-Smad2/3/4-ZEB signaling.Open life sciences · 2022Article
- Concurrent YAP/TAZ and SMAD signaling mediate vocal fold fibrosis.Scientific reports · 2021Article
- Nuclear Receptor Nur77 Controls Cardiac Fibrosis through Distinct Actions on Fibroblasts and Cardiomyocytes.International journal of molecular sciences · 2021Article
- Complex fibroblast response to glucocorticoids may underlie variability of clinical efficacy in the vocal folds.Scientific reports · 2020Article
- Porcine Vocal Fold Lamina Propria-Derived Biomaterials Modulate TGF-β1-Mediated Fibroblast Activation in Vitro.ACS biomaterials science & engineering · 2020Article
- Unraveling the molecular pathobiology of vocal fold systemic dehydration using an in vivo rabbit model.PloS one · 2020Article
- Phosphorylation of the glucocorticoid receptor alters SMAD signaling in vocal fold fibroblasts.The Laryngoscope · 2019Article
- The effects of cytosporone-B, a novel antifibrotic agent, on vocal fold fibroblasts.The Laryngoscope · 2018Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
objectives/hypothesisNR4A1 was recently identified as an endogenous inhibitor of transforming growth factor (TGF)-β-induced fibrosis, and the role of this nuclear receptor has not been elucidated in tissue health or the response to injury in the vocal folds. Given the clinical implications of vocal fold fibrosis, we investigated NR4A1 expression during vocal fold wound healing in vivo and the regulatory roles of NR4A1 on vocal fold fibroblasts (VFFs) in vitro with the ultimate goal of developing targeted therapies for this challenging patient population. STUDY
designIn vivo and in vitro.
methodsIn vivo, the temporal pattern of NR4A1 mRNA expression was quantified following rat vocal fold injury. In vitro, the role of NR4A1 on TGF-β1-mediated transcription of genes underlying fibrosis as well as myofibroblast differentiation and collagen gel contraction was quantified in our human VFF line. Small interfering RNA was employed to alter NR4A1 expression to further elucidate this complex system.
resultsNr4a1 mRNA increased 1 day after injury and peaked at 7 days. Knockdown of NR4A1 resulted in upregulation of COL1A1 and TGF-β1, with TGF-β1 stimulation (both P < .001) in VFFs. NR4A1 knockdown also resulted in increased α-smooth muscle actin-positive cells (P = .013) and contraction (P = .002) in response to TGF-β1.
conclusionsNR4A1 has not been described in vocal fold health or disease. Upregulation of TGF-β following vocal fold injury was concurrent with increased NR4A1 expression. These data provide a foundation for the development of therapeutic strategies given persistent TGF-β signaling in vocal fold fibrosis. LEVEL OF EVIDENCE: N/A Laryngoscope, 127:E317-E323, 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.