ArticleInternational journal of molecular sciences2022
ASC-J9 Blocks Cell Proliferation and Extracellular Matrix Production of Keloid Fibroblasts through Inhibiting STAT3 Signaling.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Aucubin inhibits epithelial-mesenchymal transition and angiogenesis in colorectal cancer via the HDAC6/PI3K/Akt signaling pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Advances in the interplay between mechanical forces and inflammatory immunity in keloid formation.Frontiers in immunology · 2026Review
- Properties and medical applications of the Euphorbiaceae family and their bioproducts: a patent review.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Update on the Pathogenesis of Keloid Formation.JID innovations : skin science from molecules to population health · 2024Review
- Comprehensive Insights into Keloid Pathogenesis and Advanced Therapeutic Strategies.International journal of molecular sciences · 2024Review
- Insights into How Plant-Derived Extracts and Compounds Can Help in the Prevention and Treatment of Keloid Disease: Established and Emerging Therapeutic Targets.International journal of molecular sciences · 2024Review
- Review
- An updated review of the immunological mechanisms of keloid scars.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Keloids are a fibrotic skin disorder caused by abnormal wound healing and featuring the activation and expansion of fibroblasts beyond the original wound margin. Signal transducer and activator of transcription 3 (STAT3) has been found to mediate the biological functions of keloid fibroblasts (KFs). Therefore, we aimed to demonstrate whether ASC-J9, an inhibitor of STAT3 phosphorylation, can suppress the activation of KFs. Western blotting results showed that ASC-J9 inhibited the levels of COL1A1 and FN1 proteins, which were upregulated in KFs, by decreasing the expression of pSTAT3 and STAT3. RNA sequencing and in vitro studies further demonstrated that ASC-J9 treatment of KFs reduced cell division, inflammation, and ROS generation, as well as extracellular matrix (ECM) synthesis. ELISA assays verified that ASC-J9 treatment significantly mitigated IL-6 protein secretion in KFs. Transmission electron microscopy images revealed that ASC-J9 induced the formation of multilamellar bodies in KFs, which is associated with autophagy-related signaling. These results suggested that inhibiting a vicious cycle of the ROS/STAT3/IL-6 axis by ASC-J9 may represent a potential therapeutic approach to suppress cell proliferation and ECM production in KFs.
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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.