• Ling Chen, Yiliang Yin, Jingyun Li, Qian Li, Zezhang Zhu, and Jun Li.
• Division of Spine Surgery, Department of Orthopedic Surgery, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing 210008, China; Department of Plastic & Cosmetic Surgery, Women's Hospital of Nanjing Medical University (Nanjing Women and Children's Healthcare Hospital), Nanjing 210004, China.
• Burns. 2024 Dec 12; 51 (2): 107353107353.

AbstractThe etiology of hypertrophic scar formation continues to elude researchers, despite advancements in the understanding of skin scarring. Several long non-coding RNAs (lncRNAs) have been implicated in the pathogenesis of hypertrophic scars, yet the role and molecular mechanisms of LINC00525 in this process remain unclear. This study demonstrates that LINC00525 enhances cell proliferation and collagen expression through knockdown and overexpression techniques. Further analysis, including nuclear and cytoplasmic localization studies, RNA pull-down assays, bioinformatics predictions, and PCR validation, reveals that LINC00525 interacts with miR-29a-5p. The downregulation of LINC00525 enhances the expression of miR-29a-5p and suppresses the TGF-β/Smad signaling pathway. Additionally, TGF-β1 induces the upregulation of LINC00525. Collectively, these findings indicate that LINC00525 operates through a feedforward mechanism to regulate TGF-β signaling in hypertrophic scar fibroblasts. This research offers novel insights for the prevention and treatment of scars.Copyright © 2024 Elsevier Ltd and International Society of Burns Injuries. All rights reserved.

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