Heterozygous MALAT1-deficient ApoE-/- mice displayed massive immune system dysregulation and atherosclerosis within 2 months even when kept on normal diet.
Here, we discuss the flow-sensitive lncRNA STEEL along with other lncRNAs studied in the context of vascular pathophysiology and atherosclerosis such as MALAT1, MIAT1, ANRIL, MYOSLID, MEG3, SENCR, SMILR, LISPR1, and H19.
The effect of MALAT1 on atherosclerosis was determined in apolipoprotein E-deficient (Apoe<sup>-</sup><sup>/-</sup>) MALAT1-deficient (Malat1<sup>-/-</sup>) mice that were fed with a high-fat diet and by studying the regulation of MALAT1 in human plaques.
This study was designed to explore the role of exosomes from oxidized low-density lipoprotein (oxLDL)-treated vascular endothelial cells (VECs) in regulating DCs maturation in AS, and to elucidate whether MALAT1 was involved in this process.
Our study revealed that the pathological EndMT required the activation of the MALAT1-dependent Wnt/β-catenin signaling pathway, which may be important for the onset of atherosclerosis.
Furthermore, lncRNA MALAT1 knockdown significantly inhibited high glucose-induced pyroptosis in EA.hy926 cells, which may critically influence atherosclerosis.
In all, our data suggested that MALAT1 might play a protective role at least partly by sponging miR-216a-5p and regulating Beclin-1, highlighting that MALAT1 might be a potential therapeutic target of AS.