ArticleHeliyon2024
CLC-3 regulates TGF-β/smad signaling pathway to inhibit the process of fibrosis in hypertrophic scar.
Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 9 citations in OpenAlex.
- Molecular Targets in Modern Cosmetic Science.Molecules (Basel, Switzerland) · 2026Review
- Flaxseed oil and probiotics protect against induced nonalcoholic fatty liver disease (NAFLD) in male rats.Open life sciences · 2026Article
- Prophylactic adjuvant therapy for postoperative recurrence of urethral stricture: a narrative review.Translational andrology and urology · 2025Review
- Autologous Fat Granules Combined with PRP Treat Hypertrophic Scars Through TGF-β/Smad Signaling Pathway.Aesthetic plastic surgery · 2025Article
- Chrysin inhibits hypertrophic scar formation through TGF-β/Smad signaling pathways.Journal of molecular histology · 2025Article
- Therapeutic Potential of Endothelial Progenitor Cells in Angiogenesis and Cardiac Regeneration: A Systematic Review and Meta-Analysis of Rodent Models.Advanced pharmaceutical bulletin · 2025Review
- Mesenchymal stem cell exosomes regulate TGFβ/Smad3 by decreasing the METTL3-NEAT1 axis to inhibit scar progression after breast surgery.Journal of molecular histology · 2025Article
- HOXC10 promotes hypertrophic scar fibroblast fibrosis through the regulation of STMN2 and the TGF-β/Smad signaling pathway.Histochemistry and cell biology · 2024Article
- Isorhamnetin inhibits hypertrophic scar formation through TGF-β1/Smad and TGF-β1/CREB3L1 signaling pathways.Heliyon · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: To study the role and mechanism of chloride channel-3 (ClC-3) in the formation of hypertrophic scar by constructing ClC-3 interference vectors and examining their effects on human hypertrophic scar fibroblasts (HSFB). Methods: Human HSFB and human normal skin fibroblasts (NSFB) were used in this study, and ClC-3 interference vectors were constructed to transfect cells. ClC-3 inhibitors NPPB and Tamoxifen were used to treat cells. Cell migration and the expression of TGF-β/Smad, CollagenⅠ,CollagenⅢ were examined to explore the role of ClC-3 in the formation of hypertrophic scar. Results: Compared with the normal skin tissue, the positive expression of ClC-3 and TGF-β in the scar tissue was significantly increased. The relative expression of ClC-3 and TGF-β1 in HSFB cells was higher than that in NSFB cells. Interfering with the expression of CLC-3 can inhibit the migration of HSFB cells and the expression of TGF- β/Smad, CollagenⅠ/Ⅲ. The experiment of HSFB cells treated by CLC-3 inhibitors can also obtain similar results. Conclusion: Inhibiting CLC-3 can reduce the formation of hypertrophic scars.
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