ArticlePloS one2009
Rac inhibition reverses the phenotype of fibrotic fibroblasts.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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
29 citing papers in PubMed, 49 citations in OpenAlex.
- Therapeutic interleukin-6 blockade reverses transforming growth factor-beta pathway activation in dermal fibroblasts: insights from the faSScinate clinical trial in systemic sclerosis.Annals of the rheumatic diseases · 2018Trial
- Aortic carboxypeptidase-like protein potentiates β1 integrin signaling in mesenchymal progenitors.Life science alliance · 2026Article
- The Pro-Fibrotic Response to Lens Injury Is Signaled in a PI3K Isoform-Specific Manner.Biomolecules · 2022Article
- Rho GTPase signaling in rheumatic diseases.iScience · 2022Review
- Article
- The Role of Rho GTPases During Fibroblast Spreading, Migration, and Myofibroblast Differentiation in 3D Synthetic Fibrous Matrices.Cellular and molecular bioengineering · 2021Article
- Downregulation of miR‑483‑5p inhibits TGF‑β1‑induced EMT by targeting RhoGDI1 in pulmonary fibrosis.Molecular medicine reports · 2021Article
- Verteporfin inhibits the persistent fibrotic phenotype of lesional scleroderma dermal fibroblasts.Journal of cell communication and signaling · 2021Article
- Cooperative signaling between integrins and growth factor receptors in fibrosis.Journal of molecular medicine (Berlin, Germany) · 2021Review
- Fibrotic expression profile analysis reveals repurposed drugs with potential anti-fibrotic mode of action.PloS one · 2021Article
- Article
- Conjunction junction, what's the function? CCN proteins as targets in fibrosis and cancers.American journal of physiology. Cell physiology · 2020Review
- RhoB loss induces Rac1-dependent mesenchymal cell invasion in lung cells through PP2A inhibition.Oncogene · 2016Article
- Regulation of valve endothelial cell vasculogenic network architectures with ROCK and Rac inhibitors.Microvascular research · 2015Article
- Developing novel anti-fibrotic therapeutics to modulate post-surgical wound healing in glaucoma: big potential for small molecules.Expert review of ophthalmology · 2015Review
- Actin-mediated gene expression depends on RhoA and Rac1 signaling in proximal tubular epithelial cells.PloS one · 2015Article
- CXCL12 induces connective tissue growth factor expression in human lung fibroblasts through the Rac1/ERK, JNK, and AP-1 pathways.PloS one · 2014Article
- TGFβ receptor I transactivation mediates stretch-induced Pak1 activation and CTGF upregulation in mesangial cells.Journal of cell science · 2013Article
- IntegrinAdvances in wound care · 2013Review
- FAK-related nonkinase is a multifunctional negative regulator of pulmonary fibrosis.The American journal of pathology · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundFibrosis, the excessive deposition of scar tissue by fibroblasts, is one of the largest groups of diseases for which there is no therapy. Fibroblasts from lesional areas of scleroderma patients possess elevated abilities to contract matrix and produce alpha-smooth muscle actin (alpha-SMA), type I collagen and CCN2 (connective tissue growth factor, CTGF). The basis for this phenomenon is poorly understood, and is a necessary prerequisite for developing novel, rational anti-fibrotic strategies. METHODS AND
findingsCompared to healthy skin fibroblasts, dermal fibroblasts cultured from lesional areas of scleroderma (SSc) patients possess elevated Rac activity. NSC23766, a Rac inhibitor, suppressed the persistent fibrotic phenotype of lesional SSc fibroblasts. NSC23766 caused a decrease in migration on and contraction of matrix, and alpha-SMA, type I collagen and CCN2 mRNA and protein expression. SSc fibroblasts possessed elevated Akt phosphorylation, which was also blocked by NSC23766. Overexpression of rac1 in normal fibroblasts induced matrix contraction and alpha-SMA, type I collagen and CCN2 mRNA and protein expression. Rac1 activity was blocked by PI3kinase/Akt inhibition. Basal fibroblast activity was not affected by NSC23766.
conclusionRac inhibition may be considered as a novel treatment for the fibrosis observed in SSc.
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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.