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Myocardin-induced smooth muscle long non-coding RNA, inducer of differentiation (MYOSLID)

Target
MYOSLID
Molecular classification
Long non-coding RNA (lncRNA), Other (non-protein-coding regulatory RNA)
01

Overview

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].

Other names
MYOSLID lncRNAmyocardin-induced smooth muscle lncRNAMYOSLID RNA
02

Biological functions

Smooth muscle cell differentiationInhibition of smooth muscle cell proliferationRegulation of actin stress fiber formationModulation of TGFβ/SMAD signaling pathwayAmplification of contractile gene expression in vascular smooth muscle cells
03

Disease associations

Cardiovascular disease (impaired expression is observed in failed human arteriovenous fistula, which involves vascular remodeling)Potential cancer relevance (role in gastric cancer via miR-29c-3p sponging)
04

Biomarkers

Expression levels of MYOSLID (potential biomarker for VSMC differentiation state and vascular remodeling)

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