ArticleMolecular therapy : the journal of the American Society of Gene Therapy2024
Targeting the nuclear long noncoding transcript LSP1P5 abrogates extracellular matrix deposition by trans-upregulating CEBPA in keloids.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Identification of Epigenetic Regulator-Associated Genes in Keloid Disease Through Integrated Bulk and Single-Cell Transcriptomics With RT-qPCR Validation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Laser-induced skin microenvironment remodeling via exosomal CEBPA-mediated crosstalk between keratinocyte and fibroblast.Journal of nanobiotechnology · 2026Article
- A multifunctional nano-hydrogel attenuates skin photoaging via regulating ECM microenvironment homeostasis.Materials today. Bio · 2026Article
- Histone modifications in skin fibrosis: linking immune dysregulation, metabolic reprogramming, and persistent fibrotic remodeling.Frontiers in immunology · 2026Review
- Decoding the Causal Effects of Blood-Related Phenotypes in Hypertrophic Scars and Keloids: A Mendelian Randomization Study.Clinical, cosmetic and investigational dermatology · 2026Article
- Mesenchymal stem cells attenuate keloid pathogenesis via TGF-β1/SMAD-driven MMP9 suppression: mechanistic insights into collagen remodeling and extracellular matrix homeostasis.Blood science (Baltimore, Md.) · 2025Article
- Recent Progress in Keloid Mechanism and Treatment: A Comprehensive Review.Biomedicines · 2025Review
- IFN-γ could induce ferroptosis in keloid fibroblasts by inhibiting the expression of serpine2.Cell death discovery · 2025Article
- ALKBH3-Mediated MAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
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Abstract
Keloids are characterized by fibroblast hyperproliferation and excessive accumulation of extracellular matrix (ECM) and are a major global health care burden among cutaneous diseases. However, the function of long noncoding RNA (lncRNA)-mediated ECM remodeling during the pathogenesis of keloids is still unclear. Herein, we identified a long noncoding transcript, namely, lymphocyte-specific protein 1 pseudogene 5 (LSP1P5), that modulates ECM component deposition in keloids. First, high-throughput transcriptome analysis showed that LSP1P5 was selectively upregulated in keloids and correlated with more severe disease in a clinical keloid cohort. Therapeutically, the attenuation of LSP1P5 significantly decreased the expression of ECM markers (COL1, COL3, and FN1) both in vitro and in vivo. Intriguingly, an antifibrotic gene, CCAAT enhancer binding protein alpha (CEBPA), is a functional downstream candidate of LSP1P5. Mechanistically, LSP1P5 represses CEBPA expression by hijacking Suppressor of Zeste 12 to the promoter of CEBPA, thereby enhancing the polycomb repressive complex 2-mediated H3K27me3 and changing the chromosomal opening status of CEBPA. Taken together, these findings indicate that targeting LSP1P5 abrogates fibrosis in keloids through epigenetic regulation of CEBPA, revealing a novel antifibrotic therapeutic strategy that bridges our current understanding of lncRNA regulation, histone modification and ECM remodeling in keloids.
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