Abstract:Endothelial dysfunction is a pivotal contributor to atherosclerosis (As) pathogenesis. A comprehensive understanding of the mechanisms of endothelial dysfunction would provide novel insights into effective treatment of As. Recent advances in genome and transcripome technology have enabled researchers to further explore the molecular mechanisms of endothelial dysfunction. It has been found that the regulatory network of competitive endogenous RNA (ceRNA) mediated by long non-coding RNA (lncRNA) plays a key role in endothelial dysfunction. lncRNA acts as a “molecular sponge” for microRNA (miRNA) to block the post-transcriptional repression of miRNA on downstream target gene messenger RNA (mRNA) by binding to miRNA, thereby regulating the function and phenotypic conversion of endothelial cell (EC) lncRNA-miRNA-mRNA interactions are widely involved in play an essential role EC inflammatory responses, apoptosis, autophagy, angiogenesis, and endothelial-mesenchymal transition (EndMT). Which suggests that it may be a potential therapeutic targets for As.

Abstract:Exosomes are the means of intercellular communication, and long non-coding RNAs (lncRNA), as the cargo of exosomes, are involved in regulating various physiological and pathological processes of cardiovascular system due to their rich functions. This article reviews the relevant research on extracellular lncRNA in the field of acute myocardial infarction, summarizes the regulatory role of extracellular lncRNA, analyzes the current research status of extracellular lncRNA as a biomarker and treatment strategy for myocardial infarction, and selects potential biomarkers through sequencing information in public databases.

Abstract:Long non-coding RNA (lncRNA) is a class of RNA more than 200 nucleotides long and has no protein-coding capacity, but it plays a very important role in regulating various biological processes such as proliferation, apoptosis, migration, invasion and differentiation. It has found that lncRNA is closely related to the development of myocardial ischemia/reperfusion (I/R) injury. This review discusses the advances in the reduction of myocardial I/R injury and its possible mechanisms by lncRNA.

Abstract:Aim To explore the effect of proline/serine rich coiled coil protein 1-mediated long non-coding RNA (lncLEPIS) overexpression on blood lipid levels and the occurrence and development of atherosclerosis. Methods 16 ApoE－/－ mice were randomly divided into control group (NC group) and lncLEPIS overexpression group (lncLEPIS group), and ApoE－/－ mice fed with high-fat diet with liver lncLEPIS overexpression were constructed. Atherosclerotic plaques in mouse aorta were assessed by oil red O staining. Blood lipid levels were detected by enzyme labeling method.The mRNA expression levels of cholesterol metabolism-related genes were detected by real-time quantitative PCR. Results The plaque area/aortic area in the NC group and the lncLEPIS group were (18.6%±0.3%) and (28.0%±1.3%), and the plaque area/aortic root cross-sectional area were (7.5%±0.2%) and (17.8%±0.3%), the differences between the two groups was significant (P＜0.05). The plasma triglyceride levels of the mice in the NC group and the lncLEPIS group were (0.65±0.07) mmol/L and (0.96±0.21) mmol/L, the total cholesterol levels were (3.56±0.71) mmol/L and (7.36±0.65) mmol/L, the high density lipoprotein cholesterol levels were (1.46±0.05) mmol/L and (1.95±0.38) mmol/L, and the low density lipoprotein cholesterol levels were (2.59±0.35) mmol/L and (5.59±0.59) mmol/L, the differences between the two groups were significant (P＜0.05). Compared with the NC group, the expression level of low density lipoprotein receptor (LDLR) in the liver of mice was down-regulated by 48.4% in the lncLEPIS group, and the expression level of proprotein convertase subtilisin/kexin 9 (PCSK9) was up-regulated by 62.8% (P＜0.05). Conclusion Overexpression of lncLEPIS reduces the expression of LDLR, promotes the expression of PCSK9, increases the level of plasma LDLC, and promotes the occurrence and development of atherosclerosis.

Abstract:Aim To investigate the effect of long non-coding RNA (lncRNA) HOX transcript antisense RNA (HOTAIR) on coronary heart disease (CHD) and its mechanism. Methods The expression levels of lncRNA HOTAIR, microRNA-126 (miR-126) and Polo-like kinase 4 (PLK4) in peripheral blood samples and endothelial progenitor cells (EPC) of CHD patients and healthy volunteers were detected by quantitative real-time PCR. EPC cell viability was detected by methyl thiazolyl tetrazolium assay. Apoptosis rate was detected by flow cytometry. The expressions of autophagy-related proteins LC3-Ⅱ and Beclin1 were detected by Western blot. Cell autophagy was observed by confocal microscopy. The relationship between lncRNA HOTAIR and miR-126 was analyzed by miRcode software and dual-luciferase reporter gene assay. The relationship between miR-126 and PLK4 was analyzed by TargetScan software and dual-luciferase reporter gene assay. The effect of lncRNA HOTAIR on mammalian target of rapamycin (mTOR) pathway through miR-126 in EPC was detected by Western blot. Results The expressions of lncRNA HOTAIR and PLK4 were significantly up-regulated in CHD blood samples and EPC (P＜0.01), and the expression of miR-126 was significantly down-regulated (P＜0.01). Down-regulation of lncRNA HOTAIR or PLK4 promoted autophagy in EPC, and inhibited CHD progression. Up-regulation of lncRNA HOTAIR inhibited EPC autophagy and promoted apoptosis through miR-126.The lncRNA HOTAIR activated the mTOR pathway in EPC via miR-126. Conclusion HOTAIR/miR-126/PLK4 axis mediates autophagy in EPC and affects CHD via mTOR signaling pathway.

Abstract:Vascular calcification (VC) increases the incidence of cardiovascular events in patients with chronic kidney disease, hypertension and diabetes mellitus. However, up to now, the molecular mechanism leading to VC has not been fully elucidated, and there is a lack of effective treatment methods, so it is necessary to find new therapeutic targets.With the development of molecular biological analysis technology, non-coding RNA has become an important research hotspot. It has been reported that non-coding RNA can regulate the expressions of osteogenic gene or osteogenic inhibition gene, or regulate autophagy and aging process to regulate VC under the stimulation of VC promoting factors. This review mainly summarizes the research progress of non-coding RNA (microRNA, long non-coding RNA and circular RNA) in VC.

Abstract:Aim To investigate the effect of long non-coding RNA MIR155 host gene (lncRNA MIR155HG) on proliferation, migration, differentiation and collagen synthesis of myocardial fibroblasts and its molecular mechanism. Methods Mouse myocardial infarction model was constructed. Myocardial fibroblasts were isolated and divided into silent control group, silent MIR155HG group, silent MIR155HG and inhibitor control group, silent MIR155HG and interference miR-133a-3p group, silent MIR155HG and over-expressed Furin group. The expression levels of MIR155HG, miR-133a-3p and Furin were detected by quantitative real-time PCR. Methyl thiazolyl tetrazolium colorimetry was used to detect cell viability. Cell migration was detected by Transwell experiment. Western blot was used to detect the expressions of cyclin D1, cyclin-dependent kinase inhibitor 1A (P21), vascular endothelial growth factor (VEGF), collagen type 1 (Col-1) and α-smooth muscle actin (α-SMA). Targeting relationships between MIR155HG and miR-133a-3p, between miR-133a-3p and Furin were detected by luciferase report experiment. Results In the heart tissue of myocardial infarction model mice, MIR155HG and Furin were highly expressed, and miR-133a-3p was lowly expressed (P＜0.05). After inhibiting MIR155HG expression, the cell viability, migration cell number and cyclin D1, VEGF, Col-1, α-SMA expression levels of myocardial fibroblasts were significantly decreased, while P21 expression level was significantly increased (P＜0.05). MIR155HG targetedly regulated miR-133a-3p, and miR-133a-3p targetedly regulated Furin. Inhibition of miR-133a-3p expression and overexpression of Furin reversed the inhibition effect of inhibiting MIR155HG expression on proliferation, migration, differentiation and collagen synthesis related proteins of myocardial fibroblasts. Conclusion Inhibition of MIR155HG expression can inhibit the proliferation, migration, differentiation and collagen synthesis of myocardial fibroblasts, which may be related to the regulation of miR-133a-3p/Furin axis.

Abstract:Atherosclerosis (As) is the most common lesion of cardio-cerebrovascular disease endangering human health in the modern society. Finding the potential biomarkers during the progress of As is significant for the prevention and treatment of As-related diseases. Studies have shown that long non-coding RNA (lncRNA) can be widely involved in many cell activity regulation processes, and play a role in different stages of As development. LncRNA can be secreted into the circulatory system by exosome, micro-vesicle and apoptotic bodies. In the recent years, investigations on the circulating lncRNA in As have been reported more and more. The circulating lncRNA is expected to become the novel non-invasive biomarker to monitor the progress of As.

Abstract:With the development of molecular biology technology in recent years, cardiovascular disease research entered the era of genetic testing. An increasing number of studies shows that, lncRNA not only has close relationship with cardiovascular disease, but also plays a key role in cardiovascular disease of the regulation mechanism. This review focuses on the association between lncRNA and cardiovascular disease.