Smooth muscle-induced long noncoding RNA enhances replication (SMILR)

Smooth muscle-induced long noncoding RNA enhances replication (SMILR) is a long intergenic noncoding RNA (lincRNA) that is strongly induced in vascular smooth muscle cells (VSMCs) in response to proliferative stimuli such as interleukin-1α and platelet-derived growth factor. SMILR does not code for protein but functions as a regulatory RNA, enhancing VSMC proliferation by promoting cell cycle gene expression. Mechanistically, it interacts with cell cycle-associated mRNAs and proteins, including the mRNA for mitotic regulator CENPF and RNA-binding protein Stau1. SMILR levels are increased in unstable atherosclerotic plaques and patient plasma with elevated inflammation, and suppression of SMILR reduces cell proliferation and may help prevent vascular diseases associated with excessive smooth muscle growth. This makes SMILR a promising RNA-based therapeutic target and a candidate biomarker for proliferative vascular disorders[1][3][5][7].

Other names

SMILRSmooth muscle-induced lncRNA enhancer of proliferationSmooth muscle-enriched long noncoding RNAEnsembl: RP11-94A24.1

Research targeting SMILR generally aims to suppress its expression (e.g., by RNA interference), thereby reducing vascular smooth muscle cell proliferation through downregulation of mitotic regulators and HAS2 expression. The mechanistic focus is on gene expression modulation rather than classic receptor/enzyme blockade.