Skip to main content

Table 5 LncRNAs implicated in the development of atherosclerotic cardiovascular diseases

From: Expedition to the missing link: Long noncoding RNAs in cardiovascular diseases

LncRNAClinical RelevancePhysiological/pathological impactMechanism involved
H19 [79, 98,99,100]↑ in VSMC of neointima and AAAEC: Improved wound healing in diabetic rats
VSMC: promotes SMC apoptosis and development of AAA
EC: Hyperglycemia-induced reduction impaired angiogenesis in diabetes through insulin PI3K-Akt pathway
VSMC: Regulate VSMC apoptosis through interaction with HIF1α and sequential p53 stabilization
MALAT1 [81,82,83, 101]↑ in VSMC and EC in response to stresses like hypoxia or high glucoseEC: Deletion delayed vessel extension in the retina revascularization, and reduced blood flow recovery after hindlimb ischemia
VSMC: Deletion restores contractile protein gene expression, improves aortic mural architecture, and inhibits experimental aneurysm growth
EC: Inhibit cell cycle progression through reducing the S-phase cyclins while increasing the cell cycle inhibitory genes P21 and P27kip1
ANRIL [95, 96]Adjacent to 9p21.3 CAD risk locusVSMC: Deleting the risk haplotype rescues VSMC stabilityVSMC: regulated cell proliferation and senescence of VSMCs either by a scaffold, guiding effector-proteins to chromatin, or by regulating miR-181a/Sirt1
MEG3 [85,86,87]Downregulated with stroke and diabetic retinaEC: Deletion results in a proangiogenic effectEC: Deletion upregulate Notch VEGF pathway-related genes
NEXN-AS1 [88]Reduced in arterial plaquesNEXN plays a protective role against development of vulnerable atherosclerotic plaques and atherosclerosisEC: inhibit endothelial activation and monocyte recruitment via the TLR4/NF-κB–mediated pathway
MANTIS [89, 90]Induced by disturbed flow;
Reduced in arterial plaques
EC: statins mediate their positive effects through the MANTISEC: flow sensitive, limit endothelial ICAM-1 expression by reducing the binding of the BRG1 at the ICAM-1 promoter
LncLSTR [102] LncLSTR deletion reduces plasma triglyceride levels by increasing hepatic expression of lipoprotein ApoC2Regulate expression of Cyp8b1, which alters the activity of bile acid receptor FXR in liver, leading to induction of ApoC2 genes
LeXis [103, 104] Reduce hepatic cholesterol biosynthesis, serum cholesterol and atherosclerotic lesionInhibit cholesterol biosynthesis as a conduit between LXR and SREBP2
MeXis [105] Deletion in mouse bone marrow cells impairs cellular responses to cholesterol overload, and accelerates atherosclerosisModulate nearby gene Abca1 expression through interacting with and guiding promoter binding of the transcriptional coactivator DDX17