Small extracellular vesicles (sEVs)-derived circular RNAs (circRNAs) could regulate gene expression in recipient cells, and dysregulation of sEVs-derived circRNAs has been implicated in several diseases. However, the expression and function of sEVs-derived circRNAs in coronary heart atherosclerotic disease (CAD) remain unknown. In this study, we investigated global changes in the expression patterns of circRNAs in sEVs from CAD-related monocytes and identified circNPHP4 as a significantly upregulated circRNA. Knockdown of circNPHP4 inhibited heterogeneous adhesion between monocytes and coronary artery endothelial cells and reduced ICAM-1 and VCAM-1 expression. Investigations of the underlying mechanisms revealed that circNPHP4 contains a functional miR-1231-binding site. Mutation of the circNPHP4-binding sites in miR-1231 abolished the interaction, as indicated by a luciferase reporter assay. Furthermore, circNPHP4 affected the expression of miR-1231 and its target gene EGFR. Overexpression of miR-1231 blocked the inhibitory effect of circNPHP4 on heterogeneous adhesion. Moreover, downregulation of miR-1231 restored heterogeneous adhesion upon inhibition by circNPHP4 silencing. Additionally, circNPHP4 overexpression was correlated with aggressive clinicopathological characteristics in CAD patients. A multivariate logistic regression model and bootstrapping validation showed that circNPHP4 overexpression had a good risk prediction capability for CAD. The decision curve analysis revealed that using the CAD nomogram that included circNPHP4 overexpression to predict the risk of CAD was beneficial. Our results suggest that sEVs-derived circNPHP4 can serve as a potential target for CAD treatments or as a potential diagnostic marker for CAD patients.
This case study demonstrates the feasibility of pacing the left bundle branch and atrial septum under transthoracic echocardiography (TTE) without fluoroscopic guidance. This technique could be useful to guide pacemaker implantation in some patients, especially pregnant women.
BackgroundEarly diagnosis and treatment significantly improve the prognosis of coronary heart disease (CHD), but no convenient screening tools are available. This study aims to find potential non-invasive screening biomarkers of coronary heart disease.MethodWe performed microarray analysis to investigate the mRNA expression levels in Small extracellular vesicles (sEVs) and screen significantly differentially expressed mRNAs in CHD patients vs. non-CHD patients. We then performed quantitative real-time polymerase chain reaction (qRT-PCR) to validate the microarray results, and we calculated the correlations between expression levels and clinicopathological data. Microarray analysis identified 72 downregulated mRNAs and 31 upregulated mRNAs in CHD patients relative to non-CHD patients.ResultsFrom the study, we found that upregulated sphingosine-1-phosphate receptor 5 (S1PR5) and downregulated carnosine synthase 1 (CARNS1) had the most significant differences between the patient group and the control group. S1PR5 expression was correlated with diabetes, heart rate, triglycerides, total cholesterol, low-density lipoprotein cholesterol, apolipoprotein B, and fasting blood glucose (P < 0.05). CARNS1 level was correlated with uric acid (UA) (P < 0.05). Overexpressed S1PR5 and downregulated CARNS1 were independent risk factors for CHD. The area under the receiver operating characteristic curve (AUC) of S1PR5 was 0.838 for diagnosing CHD; the AUC of CARNS1 was 0.883 for non-CHD; and the AUC of S1PR5 plus CARNS1 was 0.921 for CHD.ConclusionsMicroarray analysis showed that upregulated S1PR5 and downregulated CARNS1 in sEVs have the potential to become non-invasive biomarkers for CHD screening.
Background
Addison’s disease which is due to dysfunction of the adrenal gland, with abnormal secretion of glucocorticoids and mineralocorticoids, is rare. By inducing inflammation and disorders of water and electrolyte metabolism, Addison’s disease may accelerate progression of co-existed cardiovascular diseases. Addison’s disease combined with cardiovascular disease is infrequent, only 10 cases in the literature.
Case presentation
We reported a 51-year-old male patient with unstable angina pectoris and hypotension. Changes on coronary angiography within 2 years suggested rapid progression of coronary artery disease in a patient with low cardiovascular risk. An additional clue of skin hyperpigmentation, fatigue and further examination confirmed the diagnosis of Addison’s disease caused by adrenal tuberculosis. After hormone replacement treatment, the frequency and severity of the angina pectoris were alleviated significantly, as were hypotension, hyperpigmentation and fatigue.
Conclusions
The combination of Addison’s disease and coronary artery disease in one patient is rare. Addison’s disease can induce inflammation and disorders of water and electrolyte metabolism, which may further accelerate the course of coronary artery disease. Meanwhile, the hypotension in Addison’s disease may affect the coronary blood flow, which may result in an increased susceptibility to unstable angina in the presence of coronary stenosis. So, we should analyze comprehensively if the coronary artery disease progress rapidly.
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