ArticleBioscience reports2019
BTXA regulates the epithelial-mesenchymal transition and autophagy of keloid fibroblasts via modulating miR-1587/miR-2392 targeted ZEB2.
Article in Bioscience reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Mitophagy in Botulinum Toxin Type A-Induced Muscle Atrophy.Oral diseases · 2026Article
- Botulinum toxin-induced masseter muscle atrophy is associated with impaired autophagic flux without signs of apoptosis in mice.Cell death discovery · 2026Article
- Epithelial-mesenchymal transition in cutaneous fibrosis disease: from mechanisms to therapy.Frontiers in immunology · 2026Review
- Article
- Botulinum toxin on a mission to erase keloids: does the dream come true?Postepy dermatologii i alergologii · 2025Review
- Investigating the impact of botulinum toxin type a on the migration of normal human dermal fibroblasts: An in vitro wound healing assay.Journal of cosmetic dermatology · 2024Article
- Article
- Mechanisms underlying pathological scarring by fibroblasts during wound healing.International wound journal · 2023Article
- Advances in the pathogenesis and clinical application prospects of tumor biomolecules in keloid.Burns & trauma · 2022Review
- [Several problems worthy of attention in non-surgical treatment of scar].Zhonghua shao shang za zhi = Zhonghua shaoshang zazhi = Chinese journal of burns · 2021Article
- The molecular mechanism of GADD153 in apoptosis of keloid fibroblasts exposed to botulinum toxin type A.Journal of cellular and molecular medicine · 2021Article
- [Bibliometric and visual analysis of current status and trends of international research on keloids].Zhonghua shao shang za zhi = Zhonghua shaoshang zazhi = Chinese journal of burns · 2021Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Keloids are very resistant to treatment in dermatology and plastic surgical practice. The present study aimed to explore the underlying mechanism of botulinum toxin A (BTXA) treated human skin keloid fibroblasts (HSFBs) proving some new insights into keloids treatment. Expression of miR-1587 and miR-2392 were significantly down-regulated in keloid tissues and HSFBs, while the ZEB2 was a target of both and up-regulated in keloid tissues and HSFBs compared with the normal controls. BTXA could significantly increase the expression of miR-1587 and miR-2392 but decrease the expression of ZEB2. BTXA could significantly inhibit the proliferation, cell cycle, and migration and promote apoptosis and autophagy of HSFBs; however, miR-1587 and miR-2392 inhibitors could reverse these effects of BTXA on HSFBs. Silencing ZEB2 could significantly attenuate the effects of miR-1587 and miR-2392 inhibitors in promoting cell proliferation and migration and suppressing apoptosis and autophagy of HSFBs after treating with BTXA. BTXA could suppress the proliferation and migration and promote apoptosis and autophagy of HSFBs via modulating miR-1587/miR-2392 targeted ZEB2.
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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.