ArticleJournal of molecular histology2018
miR-155 inhibits the formation of hypertrophic scar fibroblasts by targeting HIF-1α via PI3K/AKT pathway.
Article in Journal of molecular histology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis 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.
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Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.
- In Vivo Models for Hypertrophic Scars-A Systematic Review.Medicina (Kaunas, Lithuania) · 2022Pooled it
- HIF-1α/NREP axis promotes hypertrophic scar fibroblast proliferation and collagen deposition via activation of the TGF-β1/Smad pathway.Biology direct · 2026Article
- Research Advances in Therapeutic Strategies and Drug Delivery Systems for Pathological Scars.Pharmaceutics · 2026Review
- Self-organizing three-dimensional dermal papilla cell spheroids yield therapeutic extracellular vesicles that target hypertrophic scar regression via the miR-26a-5p/CCNE2 axis.Burns & trauma · 2026Article
- Therapeutic Potential of Modulating Gene-MicroRNA Crosstalk in Burn Injury.International journal of molecular sciences · 2025Review
- Fibrotic Disease of the Skin and Lung: Shared Pathways, Environmental Drivers, and Therapeutic Opportunities in a Changing Climate.International journal of molecular sciences · 2025Review
- Circadian Gene NPAS2 Relieves Hypertrophic Scar Formation via CDC25A-Mediated Fibroblasts Activity.Journal of cellular and molecular medicine · 2025Article
- Fibroblast PI3K/AKT signaling and extracellular matrix homeostasis: mechanisms, targets, and delivery challenges.Frontiers in cell and developmental biology · 2025Review
- The PI3K/AKT/mTOR pathway in scar remodeling and keloid formation: mechanisms and therapeutic perspectives.Frontiers in pharmacology · 2025Review
- Administration of a combination of COX-2/TGF-β1 siRNAs induces hypertrophic scar fibroblast apoptosis through a TP53 mediated caspase pathway.Scientific reports · 2024Article
- Cell-cell interactions in the heart: advanced cardiac models and omics technologies.Stem cell research & therapy · 2024Review
- Natural products for the treatment of hypertrophic scars: Preclinical and clinical studies.Heliyon · 2024Review
- Article
- Mechanisms underlying pathological scarring by fibroblasts during wound healing.International wound journal · 2023Article
- Macrophages in cardiac remodelling after myocardial infarction.Nature reviews. Cardiology · 2023Review
- [Research advances on the role and mechanism of microRNA in hypertrophic scar].Zhonghua shao shang yu chuang mian xiu fu za zhi · 2023Article
- Up-regulation of miR-155 protects against chronic heart failure by inhibiting HIF-1α.American journal of translational research · 2023Article
- Knockdown of lncRNA-NEAT1 expression inhibits hypoxia-induced scar fibroblast proliferation through regulation of the miR-488-3p/COL3A1 axis.Experimental and therapeutic medicine · 2022Article
- miR-155 down-regulation protects the heart from hypoxic damage by activating fructose metabolism in cardiac fibroblasts.Journal of advanced research · 2022Article
- Transition of autophagy and apoptosis in fibroblasts depends on dominant expression of HIF-1α or p53.Journal of Zhejiang University. Science. B · 2022Article
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 1 country.
Funding
Abstract
Hypertrophic scar (HS) is a serious skin fibrotic disease characterized by the excessive proliferation of fibroblasts and often considered as a kind of benign skin tumor. microRNA-155 (miR-155) is usually served as a promising marker in antitumor therapy. In view of the similarities of hypertrophic scar and tumor, it is predicted that miR-155 may be a novel therapeutic target in clinical trials. Here we found the expression levels of miR-155 was gradually down regulated and HIF-1α was upregulated in HS tissue and HS derived fibroblasts (HFs). And cell proliferation was inhibited when miR-155 was overexpressed or HIF-1α was silenced. Moreover, overexpression of miR-155 in HFs could reduce the expression of collagens in vitro and inhibit the collagen fibers arrangement in vivo, whereas miR-155 knockdown gave opposite results. Furthermore, we found that miR-155 directly targeted the HIF-1α, which could also independently inhibit the expression of collagens in vitro and obviously improved the appearance and architecture of the rabbit ear scar in vivo when it was silencing. Finally, we found that PI3K/AKT pathway was enrolled in these processes. Together, our results indicated that miR-155 was a critical regulator in the formation and development of hypertrophic scar and might be a potential molecular target for hypertrophic scar therapy.
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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.