ArticleInternational journal of molecular medicine2019
Botulinum toxin type A prevents the phenotypic transformation of fibroblasts induced by TGF‑β1 via the PTEN/PI3K/Akt signaling pathway.
Article in International journal of molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04383912 (Onabotulinum Toxin A to Improve Direct Brow Lift Outcomes), which is not on this map. Cited by 25 papers, 2 of them syntheses that pooled it.
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.
Onabotulinum Toxin A to Improve Direct Brow Lift Outcomes
Who cites it
25 citing papers in PubMed, 2 syntheses or guidelines pooled it, 28 citations in OpenAlex.
- Add-on benefits of botulinum toxin type A in combination or sequential therapies for scar management: a systematic review and meta-analysis.Frontiers in pain research (Lausanne, Switzerland) · 2026Pooled it
- Network Meta-Analysis of Different Clinical Commonly Used Drugs for the Treatment of Hypertrophic Scar and Keloid.Frontiers in medicine · 2021Pooled it
- Clinical Efficacy Analysis of Botulinum Toxin Type A Combined with Superficial Radiotherapy after Chest Keloid Surgery.Aesthetic plastic surgery · 2025Trial
- Comparison of dual-plane micro-drop injection of botulinum toxin type A with two traditional methods for treating hypertrophic scars in the tension zone: A long-term clinical application study.Journal of cosmetic dermatology · 2024Trial
- Trial
- Botulinum Toxin Type A Alleviates Hypertrophic Scar Formation in a Rabbit Ear Model by Inhibiting the TGF-β1/Smad Pathway.Aesthetic plastic surgery · 2026Article
- Epithelial-mesenchymal transition in cutaneous fibrosis disease: from mechanisms to therapy.Frontiers in immunology · 2026Review
- Engineered Exosomes Complexed with Botulinum Toxin Type A for Enhanced Anti-Aging Effects on Skin.Biology · 2025Article
- Methionine Restriction Attenuates Scar Formation in Fibroblasts Derived from Patients with Post-Burn Hypertrophic Scar.International journal of molecular sciences · 2025Article
- Kynurenine acts as a signaling molecule to attenuate pulmonary fibrosis by enhancing the AHR-PTEN axis.Journal of advanced research · 2025Article
- Advances in Etiology and Prevention of Capsular Contracture After Breast Implantation.Aesthetic plastic surgery · 2025Review
- The PI3K/AKT/mTOR pathway in scar remodeling and keloid formation: mechanisms and therapeutic perspectives.Frontiers in pharmacology · 2025Review
- Botulinum toxin combined with static progressive stretching improves fibrous stiffness of knee joint in rats through TGF-β1/Smad pathway.Biomolecules & biomedicine · 2024Article
- Botulinum toxin type A inhibits the formation of hypertrophic scar through the JAK2/STAT3 pathway.Biomolecules & biomedicine · 2024Article
- PTEN in kidney diseases: a potential therapeutic target in preventing AKI-to-CKD transition.Frontiers in medicine · 2024Review
- Botulinum neurotoxins: Future innovations.Medicine · 2023Article
- Comparing the Efficacy of Multiple Drugs Injection for the Treatment of Hypertrophic Scars and Keloid: A Network Meta-Analysis.Aesthetic plastic surgery · 2023Review
- LncRNA FPASL suppresses fibroblast proliferation through its DNA methylation via DNMT3b in hypertrophic scar.Acta biochimica et biophysica Sinica · 2022Article
- Electroacupuncture Attenuated Phenotype Transformation of Vascular Smooth Muscle Cells via PI3K/Akt and MAPK Signaling Pathways in Spontaneous Hypertensive Rats.Chinese journal of integrative medicine · 2022Article
- [Several problems worthy of attention in non-surgical treatment of scar].Zhonghua shao shang za zhi = Zhonghua shaoshang zazhi = Chinese journal of burns · 2021Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypertrophic scar (HS) is a common type of dermatosis. Botulinum toxin type A (BTXA) can exert an anti‑HS effect; however, the regulatory mechanisms underlying this effect remain unclear. Thus, the aim of this study was to examine the effects of BTXA on phosphatase and tensin homolog deleted on chromosome ten (PTEN) expression and the fibroblast phenotypic transformation induced by transforming growth factor (TGF)‑β1, which is an important regulatory factor involved in the process of HS. For this purpose, fibroblasts were treated with various concentrations of BTXA and then treated with 10 ng/ml of TGF‑β1 with gradient concentrations of BTXA. The proliferation and apoptosis of fibroblasts were measured by cell counting kit‑8 assay (CCK‑8) and flow cytometry, respectively. PTEN methylation was analyzed by methylation‑specific PCR (MSP) and DNA methyltransferase (DNMT) activity was determined using a corresponding kit. RT‑qPCR and western blot analysis were performed to detect the transcription and translation levels. The results revealed that BTXA suppressed the proliferation and increased the apoptosis of fibroblasts treated with TGF‑β1 in a dose‑dependent manner. BTXA in combination with TGF‑β1 suppressed the expression of molecules related to the extracellular matrix (ECM), epithelial‑mesenchymal transition (EMT) and apoptosis. BTXA reduced the PTEN methylation level and downregulated the expression levels of methylation‑associated genes. BTXA also inhibited the phosphorylation of phosphoinositide 3‑kinase (PI3K) and Akt. On the whole, the findings of this study indicate that BTXA may inhibit fibroblast phenotypic transformation by regulating PTEN methylation and the phosphorylation of related pathways. The findings of this study can provide a theoretical basis for HS treatment.
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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.