ArticleCurrent medical science2018
Increased Cthrc1 Activates Normal Fibroblasts and Suppresses Keloid Fibroblasts by Inhibiting TGF-β/Smad Signal Pathway and Modulating YAP Subcellular Location.
Article in Current medical science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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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.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- CTHRC1Frontiers in immunology · 2026Article
- Meox1 Promotes Cardiac Fibrosis and Pathological Remodeling following Myocardial Infarction through Cthrc1/p-Smad2/3 Signaling.International journal of biological sciences · 2026Article
- 3D keloid spheroid model: Development and application for personalized drug response prediction.Communications biology · 2024Article
- Review
- Cthrc1 deficiency aggravates wound healing and promotes cardiac rupture after myocardial infarction via non-canonical WNT5A signaling pathway.International journal of biological sciences · 2023Article
- Keloid Core Factor CTRP3 Overexpression Significantly Controlled TGF-Disease markers · 2023Article
- An updated review of the immunological mechanisms of keloid scars.Frontiers in immunology · 2023Review
- Involvement of METTL3/mJournal of molecular histology · 2021Article
- Integrated bioinformatics analysis of core regulatory elements involved in keloid formation.BMC medical genomics · 2021Article
- TGF-β Pathway in Salivary Gland Fibrosis.International journal of molecular sciences · 2020Review
- Cardiac fibroblast activation during myocardial infarction wound healing: Fibroblast polarization after MI.Matrix biology : journal of the International Society for Matrix Biology · 2020Review
- Article
- Activin-mediated alterations of the fibroblast transcriptome and matrisome control the biomechanical properties of skin wounds.Nature communications · 2020Article
- The Protective Effect of Rosmarinic Acid Against Unfavorable Influence of Methylparaben and Propylparaben on Collagen in Human Skin Fibroblasts.Nutrients · 2020Article
- The Role of CTHRC1 in Regulation of Multiple Signaling and Tumor Progression and Metastasis.Mediators of inflammation · 2020Review
- Autocrine CTHRC1 activates hepatic stellate cells and promotes liver fibrosis by activating TGF-β signaling.EBioMedicine · 2019Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Keloid may induce severe impairment of life quality for the patients, although keloid is a cutaneous benign tumor. Collagen triple helix repeat containing protein 1 (Cthrc1) was identified as a novel gene that was originally found in adventitial fibroblasts after arterial injury. To address the role of Cthrc1 in keloid, the expression level of Cthrc1 was assessed in normal skin and keloid tissue, as well as in normal fibroblasts (NFs) and keloid fibroblasts (KFs) by using quantitative PCR, Western blotting and immunohistochemical analysis. The results showed that Cthrc1 was increased in keloid tissue and KFs as compared with normal skin and NFs. Meanwhile, CCK8 and Transwell assays found the cellular proliferation and migration of KFs were increased as compared with NFs. Further, to verify the function of Cthrc1 in NFs and KFs, we increased Cthrc1 expression by transfecting lentivirus (LV) vectors LV-Cthrc1. The cellular proliferation and migration, collagen synthesis and the influence on TGF-β and YAP signaling were tested. The cellular proliferation and migration were increased in NFs-Cthrc1 as compared with NFs-control. Meanwhile, YAP expression and nuclear-location was increased in NFs-Cthrc1. On the contrary, when Cthrc1 was overexpressed in KFs, the cellular migration was suppressed and YAP expression was reduced and transferred to cytoplasm in KFs-Cthrc1 as compared with KFs-control. But the expression level of collagen I was decreased and pSmad2/3 nucleus transfer was suppressed in both NFs-Cthrc1 and KFs-Cthrc1 by using Western blotting and immunofluorescence. Increased Cthrc1 activated NFs by promoting YAP nucleus translocation, whereas suppressed KFs by inhibiting YAP nucleus translocation. Enhanced Cthrc1 decreased collagen I in both NFs and KFs by inhibiting TGF-β/Smad pathway. In conclusion, Cthrc1 may play a role in the pathogenesis of keloid by inhibiting collagen synthesis and fibroblasts migration via suppressing TGF-β/Smad pathway and YAP nucleus translocation.
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