The mechanism of miRNA regulation in atrial fibrillation (AF) occurrence and development is still unclear, especially, the regulating values of coronary circulating miRNAs has not been reported. Based on our AF radiofrequency ablation clinical practice and previous miRNA study, we proposed a hypothesis that the coronary circulating miRNA might much better reflect the regulating state and metabolic level of myocardial miRNA in AF patient. To investigate the regulating values of coronary circulation miRNA, 90 AF patients were selected and compared with 90 healthy subjects, the changes of coronary circulating miRNA differential expression profile in the whole genome were observed in this study. We found out that compared with autologous peripheral blood (PB), 6 miRNAs were upregulated and 8 miRNA downregulated in AF patients’ coronary sinus blood (CSB) significantly, especially, the expression of miR-1266, miR-4279 and miR-4666a-3p were obviously increased. Compared with normal donors’ peripheral blood, 16 miRNAs were upregulated and 24 miRNAs downregulated dramatically in patients’ peripheral blood, among them, the miR-3171 decreased, but miR-892a and miR-3149 increased significantly from the early to end stages of AF. Our results indicated that the coronary circulating miRNA can really reflect the regulating values of miRNA in AF patient; the level of miRNA change in 3 types of AF may reflect the severity of AF clinical and pathophysiological advance; The miR-892a, miR-3171 and miR-3149 may be used as biomarkers for earlier diagnosis, while miR-1266, miR-4279 and miR-4666a-3p may serve as potential intervening targets for AF patient in future.

Background: Cardiac hypertrophy is a common pathological process in many cardiac diseases, and persistent cardiac hypertrophy is the main cause of heart failure and sudden cardiogenic death. Thus, it is essential to elucidate the mechanism of cardiac hypertrophy to ensure better prevention and treatment. Methods:The Human cardiac myocytes (HCMs) were incubated with 100 nmol/L Ang II (Sigma) for 48 hours to induce the in vitro cardiomyocyte hypertrophy model. The [(3H])-leucine incorporation assay was used to evaluate cardiomyocytes hypertrophy. The activities of oxidative stress related enzymes superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA) and nitric oxide (NO) were detected using corresponding detection kits following standard protocol. Targeting relationship was verified through Bioinformatics analysis and luciferase reporter gene assay. The morphological change of cardiomyocyte was observed through immunofluorescence staining. Expressions of message ribonucleic acid (mRNA) and proteins were detected by quantitative real-time polymerase chain reaction and western blot, respectively.Results: In our study, the suppressed expression of micro ribonucleic acid (miRNA)-129-5p and the elevated expression of kelch-like ECH-associated protein 1 (keap-1) were found in the angiotensin II (Ang II)-induced cardiomyocyte hypertrophy model. MiR-129-5p effectively mimics suppressed Ang II-induced hypertrophic responses and oxidative stress. The results also showed that keap-1 was a target of miR-129-5p, and that the miR-129-5p inhibitor promoted cardiomyocyte hypertrophy and oxidative stress by elevating keap-1. Additionally, small interfering RNA (siRNA)-keap-1 activated the nuclear factor erythroid2-related factor 2 (Nrf2) pathway, while the miR-129-5p inhibitor inactivated the Nrf2 pathway by further elevating keap-1. The addition of the Nrf2 pathway activator NK-252 largely weakened the promoting effects of the miR-129-5p inhibitor on the progression of cardiomyocyte hypertrophy by suppressing oxidative stress. Conclusions:In general, the results indicate that the overexpression of miRNA-129-5p protects against cardiomyocyte hypertrophy by targeting keap-1 via the Nrf2 pathway.

Objective To quantitatively analyze the association between cholesterol efflux capacity (CEC) and the risk and prognosis of coronary artery disease (CAD). Methods A systematic search of electronic databases for studies published until September 2019 was performed. Cohorts, case-control studies, and randomized controlled trials that examined the effect of CEC on the risk and prognosis of CAD were included. Results Eighteen studies with 12 685 subjects met our inclusion criteria. Among them, 14 studies reported the CEC in non-CAD and CAD groups, and eight studies reported the association between CEC and risk of CAD. Four studies reported the prognosis of stable CAD or acute coronary syndrome (ACS). In the pooled analyses, significantly decreased CEC was found in patients with stable CAD as compared with those without CAD. Decreased CEC was also present in subgroup in patients with ACS. High CEC was significantly associated with decreased risk of CAD [odds ratio (OR) = 0.65, 95% confidence interval (CI): 0.55–0.75, P < 0.001]. High CEC predicted lower all-cause mortality (OR = 0.39, 95% CI: 0.20–0.77, P = 0.007) and cardiovascular mortality (OR = 0.34, 95% CI: 0.13–0.90, P = 0.03) in patients with CAD. However, CEC failed to predict the occurrence of stroke and myocardial infraction in patients with CAD. Conclusions Decreased CEC is an independent risk factor for CAD, and it predicts all-cause and cardiovascular mortality in patients with CAD.