Expression and Mechanism of miRNA-26 in Atrial Fibrillation
XUAN Xuexi
ZHANG Hua
ZHANG Yu
ZHANG Chuanxi
WANG Mingjie
LI Jing
Abstract：Objective:To investigate the expression and mechanism of microRNA(miRNA)-26 in atrial fibrillation.Methods:A total of 98 patients with atrial fibrillation were selected,and 98 healthy individuals who underwent physical examinations at the same time were chosen as the healthy control group.Forty male C57BL/6 mice were randomly divided into the control group,the atrial fibrillation group,the overexpression miR-26a(Adv-miR-26a)group,and the overexpression miR-26b(Adv-miR-26b)group.The control group and the atrial fibrillation group of mice were intraperitoneally injected with the same volume of normal saline.The mice in the Adv-miR-26a group and the Adv-miR-26b group were respectively injected intraperitoneally with the Adv-miR-26a lentiviral overexpression vector and the Adv-miR-26b lentiviral overexpression vector.Fourteen days later,except for the control group,the other three groups the atrial fibrillation model was established and given a tail vein injection of 1 mL/kg of the mixture of acetylcholine and calcium chloride,once a day for 7 consecutive days.The levels of miR-26a and miR-26b were detected by real-time fluorescence quantitative polymerase chain reaction(RT-qPCR).The duration and induction time of atrial fibrillation in each group of mice,as well as the action potential duration,and cardiac function,included left ventricular end-diastolic diameter(LVEDD),left atrial effective refractory period(ERP),left ventricular fractional shortening(LVFS),and left ventricular ejection fraction(LVEF)were detected.Hematoxylin-eosin(HE)staining was used to observe the myocardial pathological conditions of the mice in each group.The protein levels of type Ⅰ collagen(CollagenⅠ),type Ⅲ collagen(CollagenⅢ),connective tissue growth factor(CTGF),and matrix metalloproteinase 2(MMP-2)in each group of mice were detected by Western Blot method.Results:The levels of miR-26a and miR-26b in the serum of patients with atrial fibrillation were lower than those of the healthy control group(P＜0.05).The area under the receiver operating characteristic(ROC)curve(AUC)for serum miR-26a and miR-26b levels in patients with atrial fibrillation were 0.812 and 0.784,with sensitivities of 77.49%and 76.53%,and specificities of 77.55%and 70.41%.Compared with the control group,the levels of miR-26a and miR-26b,ERP,LVFS,LVEF in the myocardial tissue and serum of the atrial fibrillation group,decreased,while APD50,APD90,LVEDD increased,and the protein expressions of CollagenⅠ,CollagenⅢ,CTGF,and MMP-2 were upregulated(P＜0.05).Compared with the atrial fibrillation group,the levels of miR-26a and miR-26b in the myocardial tissues and serum of mice in the Adv-miR-26a group and Adv-miR-26b group increased,while ERP,LVFS,and LVEF elevated.The duration of atrial fibrillation shortened,the induction time of atrial fibrillation prolonged,APD50,APD90,and LVEDD decreased,and the protein expressions of CollagenⅠ,CollagenⅢ,CTGF,and MMP-2 were downregulated(P＜0.05).Conclusion:The miR-26a and miR-26b are expressed at low levels in the serum of patients with atrial fibrillation,as well as in the myocardial tissues and serum of mice.Overexpression of miR-26a and miR-26b can improve the cardiac function and electrophysiological conditions of mice with atrial fibrillation,alleviate myocardial fibrosis,and inhibit the occurrence of atrial fibrillation.
Keywords：atrial fibrillationmicroRNAmyocardial fibrosisheart functionelectrophysiology
Publication Date：2026-03-10
Online Publishing Date：2026-03-24(First online date of this platform, not the publication date of the document)
Pages：6( 684-689 )