ArticleThe Journal of clinical investigation2008
GSK-3beta in mouse fibroblasts controls wound healing and fibrosis through an endothelin-1-dependent mechanism.
Article in The Journal of clinical investigation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 38 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
38 citing papers in PubMed, 66 citations in OpenAlex.
- Trial
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- Therapeutic effect of bosentan on 2, 4-dinitrochlorobenzene (DNCB)-induced atopic dermatitis mouse model.Archives of dermatological research · 2025Article
- Effect of Carboxymethyl chitosan-sodium alginate hydrogel loaded withFrontiers in pharmacology · 2025Article
- Modulating the extracellular matrix to treat wound healing defects in Ehlers-Danlos syndrome.iScience · 2024Article
- 12-Cells · 2022Article
- Epithelial coxsackievirus adenovirus receptor promotes house dust mite-induced lung inflammation.Nature communications · 2022Article
- Stem Cell Therapy for Burns: Story so Far.Biologics : targets & therapy · 2021Review
- Mesenchymal-endothelial transition-derived cells as a potential new regulatory target for cardiac hypertrophy.Scientific reports · 2020Article
- Therapeutic molecular targets of SSc-ILD.Journal of scleroderma and related disorders · 2020Article
- Molecular mechanisms of arrhythmogenic cardiomyopathy.Nature reviews. Cardiology · 2019Review
- Scar management in burn injuries using drug delivery and molecular signaling: Current treatments and future directions.Advanced drug delivery reviews · 2018Review
- Loss of GSK-3 Causes Abnormal Astrogenesis and Behavior in Mice.Molecular neurobiology · 2016Article
- FKBP51 inhibits GSK3β and augments the effects of distinct psychotropic medications.Molecular psychiatry · 2016Article
- Article
- A proteomics approach to identifying key protein targets involved in VEGF inhibitor mediated attenuation of bleomycin-induced pulmonary fibrosis.Proteomics · 2016Article
- Fibroblast-Specific Deletion of Hypoxia Inducible Factor-1 Critically Impairs Murine Cutaneous Neovascularization and Wound Healing.Plastic and reconstructive surgery · 2015Article
- Wnt and Notch signaling pathway involved in wound healing by targeting c-Myc and Hes1 separately.Stem cell research & therapy · 2015Article
- The GSK-3 family as therapeutic target for myocardial diseases.Circulation research · 2015Review
- Signaling in Fibrosis: TGF-β, WNT, and YAP/TAZ Converge.Frontiers in medicine · 2015Review
Corrections and comments
- Retraction · 2008-11-03False/Forged Authorship ·
- Retracted
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Glycogen synthase kinase-3 (GSK-3) is a widely expressed and highly conserved serine/threonine protein kinase encoded by 2 genes, GSK3A and GSK3B. GSK-3 is thought to be involved in tissue repair and fibrogenesis, but its role in these processes is currently unknown. To investigate the function of GSK-3beta in fibroblasts, we generated mice harboring a fibroblast-specific deletion of Gsk3b and evaluated their wound-healing and fibrogenic responses. We have shown that Gsk3b-conditional-KO mice (Gsk3b-CKO mice) exhibited accelerated wound closure, increased fibrogenesis, and excessive scarring compared with control mice. In addition, Gsk3b-CKO mice showed elevated collagen production, decreased cell apoptosis, elevated levels of profibrotic alpha-SMA, and increased myofibroblast formation during wound healing. In cultured Gsk3b-CKO fibroblasts, adhesion, spreading, migration, and contraction were enhanced. Both Gsk3b-CKO mice and fibroblasts showed elevated expression and production of endothelin-1 (ET-1) compared with control mice and cells. Antagonizing ET-1 reversed the phenotype of Gsk3b-CKO fibroblasts and mice. Thus, GSK-3beta appears to control the progression of wound healing and fibrosis by modulating ET-1 levels. These results suggest that targeting the GSK-3beta pathway or ET-1 may be of benefit in controlling tissue repair and fibrogenic responses in vivo.
Indexed as
Identifiers
What OpenQuestion holds
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.