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Fibroblast proliferation-associated long noncoding RNA (FPASL, also called fibroblast proliferation-associated lncRNA) is a long noncoding RNA involved in the negative regulation of fibroblast proliferation and the cell cycle in human tissues. FPASL is significantly downregulated in hypertrophic scar tissues, and this downregulation is mediated by promoter hypermethylation via the DNA methyltransferase DNMT3b. Overexpression of FPASL in fibroblasts leads to suppression of proliferation and induction of cell cycle arrest at the G0/G1 phase, while knockdown of FPASL promotes cell cycle progression. This suggests FPASL acts as an epigenetically regulated suppressor of fibroblast proliferation, with relevance in fibrotic diseases such as hypertrophic scar[1][3][2]. FPASL is a non-protein-coding transcript, identified in the human genome (for example, ENSG00000289059)[2]. It is not a traditional therapeutic target (such as a receptor or enzyme) but is of research interest as a potential regulator in scar formation and possibly other fibrotic diseases[1][3]. While modulation of FPASL/DNMT3b-mediated pathways may have therapeutic potential, no drugs currently target FPASL directly[1][3].
Not applicable (there are no drugs directly targeting FPASL reported as of this response)
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