The Long Non-coding Road to Atherosclerosis
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GENETICS AND GENOMICS (A.J. MARIAN, SECTION EDITOR)
The Long Non-coding Road to Atherosclerosis Tatjana Josefs 1 & Reinier A. Boon 1,2,3
# The Author(s) 2020
Abstract Purpose of Review To summarize recent insights into long non-coding RNAs (lncRNAs) involved in atherosclerosis. Because atherosclerosis is the main underlying pathology of cardiovascular diseases (CVD), the world’s deadliest disease, finding novel therapeutic strategies is of high interest. Recent Findings LncRNAs can bind to proteins, DNA, and RNA regulating disease initiation and plaque growth as well as plaque stability in different cell types such as endothelial cells (ECs), vascular smooth muscle cells (VSMCs), and macrophages. A number of lncRNAs have been implicated in cholesterol homeostasis and foam cell formation such as LASER, LeXis, and CHROME. Among others, MANTIS, lncRNA-CCL2, and MALAT1 were shown to be involved in vascular inflammation. Further regulations include, but are not limited to, DNA damage response in ECs, phenotypic switch of VSMCs, and various cell death mechanisms. Interestingly, some lncRNAs are closely correlated with response to statin treatment, such as NEXN-AS1 or LASER. Additionally, some lncRNAs may serve as CVD biomarkers. Summary LncRNAs are a potential novel therapeutic target to treat CVD, but research of lncRNA in atherosclerosis is still in its infancy. With increasing knowledge of the complex and diverse regulations of lncRNAs in the heterogeneous environment of atherosclerotic plaques, lncRNAs hold promise for their clinical translation in the near future. Keywords lncRNA . Atherosclerosis . Cardiovascular disease
Abbreviations ABCA1 ADAM ApoE ASO BMDM CCL2 CH
ATP-binding Cassette Transporter A1 A Disintegrin and Metalloproteinase Apolipoprotein E Antisense Oligonucleotides Bone Marrow-derived Macrophages C-C Motif Chemokine Ligand 2 Cholesterol
This article is part of the Topical Collection on Genetics and Genomics * Reinier A. Boon [email protected] 1
Department of Physiology, Amsterdam Cardiovascular Science, VU University, Amsterdam UMC, Postbus 7057, 1007 MB Amsterdam, The Netherlands
2
Institute for Cardiovascular Regeneration, Centre for Molecular Medicine, Goethe University, Frankfurt am Main, Germany
3
German Center for Cardiovascular Research (DZHK), Frankfurt am Main, Germany
EC EZH HCD HDLC HFD HUVEC ICAM-1 LDL-C LDLR LPL LV MMP NFIA NLRP3 NOD PBMC OE oxLDL siRNA THP-1 VSMC WD
Endothelial Cell Enhancer of Zeste Homologue High-cholesterol Diet High-density Lipoprotein Cholesterol High-fat Diet Human Umbilical Vein Endothelial Cells Intercellular Adhesion Molecule 1 Low-density Lipoprotein Cholesterol LDL Receptor Lipoprotein Lipase Lentivirus MatrixMetallopeptidase Nuclear Factor IA LRR- and Pyrin domain-containing protein 3 Peripheral Blood Mononuclear Cell Overexpression oxidized LDL small interferenceRNA human acute monocytic leukemia cell line VascularSmooth Muscle Cells Western Diet
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Introduction The fate of atherosclerosis is dependent on the phenotype
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