Abstract:Circular RNA (circRNA) is a novel class of endogenous non-coding RNA with complex biological functions, participating in various physiological and pathological processes. Due to their relatively stable stucture and tissue-specific and temporal expression patterns, circRNA have become a recent focus of biomedical research. Heart failure (HF) is characterized by impaired ventricular filling and/or ejection function caused by primary myocardial injury and cardiac overload, leading to the inability of the heart to meet the metabolic demands of the body’s tissues. It is the end stage of numerous cardiac diseases. Studies have found that circRNA may play a crucial regulatory role in the progression of HF, particularly in cardiomyocyte hypertrophy, cardiomyocyte apoptosis, autophagy and myocardial fibrosis. This review summarizes the formation, classification, functional forms, and roles in HF of circRNA, aiming to provide new insights for the prevention and treatment of HF.

Abstract:Atherosclerosis (As), as a chronic arterial wall inflammatory response in panvascular diseases, is one of the main causes of cardiovascular and cerebrovascular diseases. At present, more and more studies have shown that circular RNA (circRNA) are involved in the pathogenetic process of atherosclerosis formation and development. It can mediate microRNA (miRNA) regulation of messenger RNA (mRNA) expression in target genes. The mechanisms include endothelial cells, vascular smooth muscle cells and macrophages proliferation, migration, differentiation, apoptosis and inflammation and other processes. And it involves multiple complex signaling pathways. In this review, we comprehensively analyze the biological function of circRNA/miRNA/mRNA and its effect on As in order to provide new ideas for the diagnosis and treatment of atherosclerotic diseases.

Abstract:Aim To investigate the effect of circ_0036167 on the fibrotic phenotype of cardiac fibroblasts and the potential mechanism involved. Methods Massons trichrome staining was performed in the myocardium of patients with heart failure (HF) and healthy organ donors. Levels of circ_0036167 and its host gene of MYO9A were determined by real-time quantitative polymerase chain reaction (RT-qPCR) in the myocardium of HF patients and healthy organ donors. Actinomycin D treatment and RNase R exonuclease digestion were used to test the stability of circ_0036167 in AC16 cells. The myocardial fibroblasts (mCF) of C57BL/6 mice were infected with recombinant circ_0036167 adenovirus, and the expression of fibrosis related genes COL1A1, COL3A1 and ACTA2 were detected at RNA and protein levels.EdU staining and transwell migration assay were performed to detect the effects of circ_0036167 on mCF proliferation and migration activities. According to the results of bioinformatic prediction, RNA binding protein immunoprecipitation (RIP) assay was performed to confirm the interaction between circ_0036167 and fused in sarcoma (FUS) protein. Effect of FUS knockdown on inhibition of fibrosis-related genes expression by circ_0036167 in mCF was determined. ResultsMassons trichrome staining showed that the cardiac fibrosis was significantly increased in the myocardium of HF patients (P＜0.001). Circ_0036167 was found markedly increased in the myocardium of HF patients (P＜0.05), with no significant difference in its host gene of MYO9A. In response to actinomycin D treatment and RNase R exonuclease digestion, circ_0036167 was more stable than MYO9A. Over-expression of circ_0036167 suppressed proliferation and migration of mCF, and inhibited RNA and protein expression of fibrosis-related genes in mCF. RIP assay revealed the interaction between circ_0036167 and FUS protein. Knock-down of FUS could increase fibrosis-related genes expression (P＜0.05 or P＜0.01), and significantly attenuated the inhibitory effect of circ_0036167 on fibrosis-related gene expression in mCF(P＜0.01 or P＜0.001). Conclusion FUS mediates the anti-fibrotic effect of circ_0036167 in mCF.

Abstract:Aim To explore the role of circular RNA spindle and kinetochore-associated protein 3 (circ-SKA3) in regulating Toll-like receptor 4 (TLR4) axis in atherosclerosis (As) through miR-1303. Methods Carotid artery plaque, diseased vascular tissue, normal tissue adjacent to plaque and venous blood were collected from 30 patients with As treated by carotid endarterectomy from April 2019 to April 2022. Another 30 normal venous blood samples were collected. Microarray analysis, quantitative real-time polymerase chain reaction (qRT-PCR) and fluorescence in situ hybridization (FISH) were used to detect the expression and localization of circ-SKA3 in plaque tissue of As patients, control samples, plasma exosome, human umbilical vein endothelial cell (HUVEC) and aorta of As model mice. The relationship among circ-SKA3, miR-1303 and TLR4 was verified by bioinformatics, double luciferase reporter gene detection and RNA immunoprecipitation. The proliferation, migration and angiogenesis of HUVEC were detected by CCK-8, scratch, Transwell and angiogenesis experiments. TLR4 axis-related protein expression was detected by Western blotting. Pathological changes of aorta in As model mice was observed by Oil red O staining, HE staining and Masson staining. TLR4 expression in aorta of As model mice was detected by immunohistochemistry and immunofluorescence. Results The expression levels of circ-SKA3 and TLR4 in plaque tissue, plasma exosome, oxidized low density lipoprotein (ox-LDL) treated HUVEC and circ-SKA3, TLR4 in aortic of As model mice were up-regulated (P＜0.05), while the expression level of miR-1303 was down-regulated (P＜0.05). Functional analysis showed that circ-SKA3 promoted HUVEC damage in vitro and As progress in vivo. Mechanism analysis showed that circ-SKA3 could promote TLR4 expression by adsorbing miR-1303 by sponge. Inhibition of circ-SKA3/miR-1303/TLR4 axis can inhibit the formation of As lesions. Conclusions circ-SKA3 is overexpressed in carotid plaque, plasma exosome, ox-LDL-treated HUVEC and As model mouse aorta in As patients. circ-SKA3/miR-1303/TLR4 axis can promote the development of As model in vivo and in vitro.

Abstract:Circular RNA (circRNA), one of the crucial regulatory non-coding RNA, are rich in content, stable in nature, and widespread. They can play vital roles in the occurrence and development of vascular diseases by regulating gene expression through various mechanisms. This review summarizes the current research status of circRNA in varieties of vascular diseases to provide references for researchers in related fields.

Abstract:With the progress of genome-wide analysis and RNA sequencing technology, a variety of non-coding RNA has gradually become a research hotspot. Circular RNA (circRNA) has many cellular functions, and its expression changes are related to many pathophysiological processes and the occurrence and development of diseases. The circRNA has been proved to be an important regulator of cardiovascular diseases, such as hypertension, atherosclerosis, acute myocardial infarction, heart failure, cardiac fibrosis, etc. Therefore, circRNA is expected to be a potential therapeutic target and biomarker for cardiovascular diseases. In this review, based on the biological mechanism of circRNA, we reviewed the current research progress on circRNA as a regulatory factor and biomarker of cardiovascular diseases.

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:The incidence of acquired aortic diseases, such as aortic dissection, aortic aneurysm and multiple aortitis, is increasing year by year, with a tendency to become common and frequently occurring diseases. These diseases are often in critical condition, difficult to treat and with high risk of operation. However, the molecular mechanism of their pathological process is still unclear. Circular RNA (circRNA) has the characteristics of stability, tissue/developmental stage specificity, conservativeness and variety richness. CircRNA can bind to miRNA or protein, selectively regulate gene splicing or transcription and protein translation, etc. Many studies have found the presence of specific circRNA in acquired aortic diseases, so it is speculated that circRNA may be a potential biomarker and therapeutic target for acquired aortic diseases. This article will review the origin, biological characteristics, functions of circRNA, and some circRNAs which may be involved in the regulation of the molecular mechanisms of acquired aortic diseases.