Inhibition of MAPK14 Improves Ang Ⅱ-Induced Atrial Fibrillation by Reducing Mitophagy
Objective To explore the role and potential mechanism of mitogen-activation protein kinase 14(MAPK14)in angiotensin Ⅱ(Ang Ⅱ)-induced atrial fibrillation(AF)in rats.Methods To establish a rat model of AF susceptibility induced by Ang Ⅱ,SB203580 was used to inhibit the expression of MAPK14.The left atrial dimension and left ventricular ejection fraction were evaluated by color Doppler ultrasound.Electrophysiological indexes such as atrial effective refractory period,AF induction rate and average duration of AF were measured by electrophysiological instrument.The structure of mitochondria was observed by transmission electron microscope.The degree of left atrial fibrosis was detected by Masson staining.The expression of LC3 was detected by immunohistochemical staining.The expression levels of MAPK14,p-MAPK14,mitophagy markers parkin and P62 were detected by Western blot.Results Compared with the control group,the expression of MAPK14 and p-MAPK14 in atrial tissue of AF rats was up-regulated in Ang Ⅱ group(P＜0.005).Compared with Ang Ⅱgroup,inhibition of MAPK14 could improve the induction rate of AF and the duration of AF(P＜0.000 5),reduce mitophagy in rat atrium(P＜0.05),and significantly improve the structural damage of heart and mitochondrial(P＜0.05).Conclusion Inhibition of MAPK14 could improve Ang Ⅱ-induced AF of rats by reducing mitophagy.
Atrial fibrillationMitophagyMitogen-activation protein kinase 14Angiotensin Ⅱ
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