Table 5 LncRNAs implicated in the development of atherosclerotic cardiovascular diseases

H19 [79, 98,99,100]

↑ in VSMC of neointima and AAA

EC: 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 glucose

EC: 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 locus

VSMC: Deleting the risk haplotype rescues VSMC stability

VSMC: 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 retina

EC: Deletion results in a proangiogenic effect

EC: Deletion upregulate Notch VEGF pathway-related genes

NEXN-AS1 [88]

Reduced in arterial plaques

NEXN plays a protective role against development of vulnerable atherosclerotic plaques and atherosclerosis

EC: 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 MANTIS

EC: 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 ApoC2

Regulate 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 lesion

Inhibit 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 atherosclerosis

Modulate nearby gene Abca1 expression through interacting with and guiding promoter binding of the transcriptional coactivator DDX17