ArticleClinical, cosmetic and investigational dermatology2025
LncRNA PVT1 Promotes the Progress of Hypertrophic Scar via Regulating the Proliferation and Migration of Myofibroblasts Through Targeting miR-29a-3p/STAT3.
Article in Clinical, cosmetic and investigational dermatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed.
- Dual Functionality of miRNAs During HIV Infection: From Viral Genome Suppression to Immune Response Modulation.Epigenomes · 2026Review
- The long non-coding RNA PVT1 promotes keratinocyte proliferation and inflammation in psoriasis by targeting miR-485-5p.Journal of molecular histology · 2026Article
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Hypertrophic scar (HS) is a common clinical disease during skin injury recovery. Although medicines have been listed for treatment, none are universally effective, and the details of the underlying molecular regulation are yet to be revealed. This research was aimed at exploring the clinical value of lncRNA PVT1 in HS formation and its potential mechanisms in human hyperplastic scar myofibroblasts (HSFs). Patients and Methods: Fifty-seven HS patients were enrolled. RT-qPCR was conducted to examine the RNA levels of lncRNA PVT1, miR-29a-3p and STAT3. CCK-8, Transwell, and flow cytometry were used to analyze cell proliferation, migration, and apoptosis. The targeting relationship of PVT1/miR-29a-3p and miR-29a-3p/STAT3 was proved by the dual luciferase reporter. Results: Relative expression of lncRNA PVT1 in human HS tissues was higher compared with normal tissues. LncRNA PVT1 silencing slowed proliferation and migration and accelerated apoptosis in human HSFs. miR-29a-3p was downregulated in human HS tissues, which was negatively correlated with PVT1 levels. LncRNA PVT1 was covalently bound to miR-29a-3p. miR-29a-3p played an important role in the proliferation, migration, and apoptosis of human HSFs. miR-29a-3p inhibitor rescued the negative influence of lncRNA PVT1 silencing on cells. STAT3 was covalently linked to miR-29a-3p. Conclusion: LncRNA PVT1 was a potential biomarker for HS and regulated the biological behavior of human HSFs via miR-29a-3p/STAT3.
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