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MYOSLID is a vascular smooth muscle cell (VSMC)-selective long non-coding RNA that is transcriptionally induced by myocardin and serum response factor (SRF), as well as by TGFβ/SMAD pathways[1][3][4]. Predominantly localized in the cytoplasm, MYOSLID promotes VSMC differentiation and suppresses VSMC proliferation, partly by facilitating actin fiber formation and enabling the nuclear translocation of MRTF-A (MKL1), thereby enhancing expression of contractile genes[1]. MYOSLID is downregulated in the context of vascular pathologies marked by loss of VSMC differentiation (e.g., failed arteriovenous fistulas)[1][3][4]. It functions through non-coding mechanisms, including possible sponging of microRNAs (such as miR-29c-3p in gastric cancer), and it positively modulates TGFβ1-induced SMAD2 phosphorylation and smooth muscle contractile phenotype[2][4]. MYOSLID is the first described CArG-SRF-MYOCD dependent lncRNA specific to VSMCs and is being studied as a potential molecular target for vascular disease treatment and modulation of smooth muscle cell phenotype[1][3][4].
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