[1]王璐 桑婉玥 简易 韩亚凡 王菲菲 李耀东.抑制MAPK14通过减轻线粒体自噬改善AngⅡ诱导的心房颤动[J].心血管病学进展,2024,(4):373.[doi:10.16806/j.cnki.issn.1004-3934.2024.04.019]
 WANG Lu,SANG Wanyue,JIAN Yi,et al.Inhibition of MAPK14 Improves Ang-Induced Atrial Fibrillation by Reducing Mitochondrial Autophagy[J].Advances in Cardiovascular Diseases,2024,(4):373.[doi:10.16806/j.cnki.issn.1004-3934.2024.04.019]
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抑制MAPK14通过减轻线粒体自噬改善AngⅡ诱导的心房颤动()
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《心血管病学进展》[ISSN:51-1187/R/CN:1004-3934]

卷:
期数:
2024年4期
页码:
373
栏目:
论著
出版日期:
2024-04-25

文章信息/Info

Title:
Inhibition of MAPK14 Improves Ang-Induced Atrial Fibrillation by Reducing Mitochondrial Autophagy
作者:
王璐1 桑婉玥1 简易 1 韩亚凡 2 王菲菲1 李耀东 1
(1.新疆医科大学第一附属医院心脏中心起搏电生理科 新疆心电生理与心脏重塑重点实验室,新疆 乌鲁木齐 830054;2. 山东第一医科大学医学科技创新中心,实验动物学院(省实验动物中心)
Author(s):
WANG Lu1SANG Wanyue1JIAN Yi1HAN Yafan2WANG Feifei1LI Yaodong1
(1.Department of Pacing and Electrophysiology,Department of Cardiac Electrophysiology and Remodeling,The First Affiliated Hospital of Xinjiang Medical University,Urumqi 830054 ,Xinjiang,China2. Medical Science and Technology Innovation Center,Shandong First Medical University,College of Laboratory Animals (Provincial Laboratory Animal Center),Affiliated Provincial Hospital,Jinan 250117,Shandong,China)
关键词:
心房颤动线粒体自噬MAPK14血管紧张素Ⅱ
Keywords:
Atrial fibrillationMitophagyMitogen activated protein kinase 14Angiotensin II
DOI:
10.16806/j.cnki.issn.1004-3934.2024.04.019
摘要:
目的??讨MAPK14在AngⅡ诱导的大鼠心房颤动(AF)中的作用及潜在机制。方法?#160 构建AngⅡ诱导的大鼠AF易感模型,使用SB203580抑制MAPK14的表达,采用彩色超声显像仪器评估左心房内径和左室射血分数等;电生理仪检测心房有效不应期、AF诱发率及AF平均持续时间等电生理指标;透射电镜观察线粒体结构;Masson染色检测左心房纤维化程度;免疫组织化学染色检测LC3表达;Western blot检测MAPK14、P-MAPK14、和线粒体自噬标志parkin及P62的表达水平。结果?#160 与对照组相比,AngⅡ组大鼠心房组织中MAPK14和P-MAPK14表达上调(均P<0.005)。与AngⅡ组相比,抑制MAPK14能够改善AF诱发率及AF持续时间(均P<0.0005),并减轻大鼠心房组织的线粒体自噬(均P<0.05),且显著改善心脏和线粒体结构受损(均P<0.05)。结论?#160 抑制MAPK14可通过减轻线粒体自噬改善AngⅡ诱导的大鼠AF。
Abstract:
Objective??o explore the role and potential mechanism of MAPK14 in AngⅡ-induced atrial fibrillation (AF) in rats. Methods??o establish a rat model of AF susceptibility induced by Ang Ⅱ,SB203580 was used to inhibit the expression of MAPK14. The left atrial diameter 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,mitochondrial autophagy markers parkin and p62 were detected by Western blot. Results?#160 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 Ⅱ group ,inhibition of MAPK14 could improve the induction rate of AF and the duration of AF (P < 0.0005) ,reduce mitophagy in rat atrium (P < 0.05) ,and significantly improve the structural damage of heart and mitochondrial (P < 0.05). Conclusion?#160 Inhibition of MAPK14 could improve AngⅡ-induced AF of rats by reducing mitophagy

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