The Potential Role and Mechanism of RBM47-Mediated Genes in Atherosclerosis

Abstract

RNA-binding motif 47 (RBM47), a hub gene in atherosclerosis, induced oxidative stress in macrophages in atherosclerosis progression by enhancing ENC1 stability via binding to the AU-rich elements (AREs). However, RBM47 promoted C-to-U editing of multiple genes, such as acyl-CoA synthetase family member 2 (ACSF2), apoB, CD36, CD170, IL-10, oxysterol binding protein like 9, and transmembrane protein 30a (TMEM30A). These genes play important roles in atherosclerosis. Thus, the role of RBM47 in atherosclerosis may be complex. Notably, ACSF2 and HECT and RLD domain containing E3 ubiquitin protein ligase 2 promoted ferroptosis. TMEM30A exhibited a “don’t eat me” signal. CD170 decreased ADAMTS13 activity. Recombinant ADAMTS-13 was undergoing phase 3 clinical trials. However, the biological significance of these genes after RNA editing, except for apoB and tight junction protein 1, is unclear. RBM47 also stabilized Axin1, Cullin 3, IL-8, Dickkopf WNT signaling pathway inhibitor 1, Kelch-like ECH-associated protein 1, and IL-10 expression by recognizing the GAUSAW (S = G/C, W = A/U) motif and AREs/GU-rich elements (GREs). However, the role of RBM47 in other genes that contain AREs and GREs, such as apoA-II, ABCA1, HMGCR, IFN-γ, IL-15, low-density lipoprotein receptor, oxidized low-density lipoprotein receptor 1, and programmed cell death 1 ligand 1, is unclear. This review focuses on the role and mechanism of RBM47-mediated genes in atherosclerosis to provide knowledge for new targets.