MAPK14/AIFM2通路调节线粒体自噬依赖性细胞凋亡改善心房颤动。

IF 4.9 2区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS
Lu Wang , Wanyue Sang , Yi Jian , Yafan Han , Feifei Wang , Subinuer Wubulikasimu , Li Yang , Baopeng Tang , Yaodong Li
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引用次数: 0

摘要

目的:探讨MAPK14/AIFM2通路在Angⅱ型心房颤动中的作用及机制。方法:建立AF大鼠模型进行体内实验,并用Angⅱ处理HL-1细胞建立离体模型。构建过表达AIFM2的HL1细胞(oeAIFM2)。使用SB203580抑制MAPK14的表达。通过体内电生理检查和分子生物学检测,探讨MAPK14在Ang II-AF模型中的作用。探讨MAPK14 / AIFM2通路在Angⅱ诱导AF中的作用。结果:MAPK14和AIFM2在Ang II诱导的AF中显著上调(P均为 )。结论:抑制MAPK14/AIFM2通路通过抑制线粒体自噬依赖性凋亡改善Ang II诱导的AF。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

MAPK14/AIFM2 pathway regulates mitophagy-dependent apoptosis to improve atrial fibrillation

MAPK14/AIFM2 pathway regulates mitophagy-dependent apoptosis to improve atrial fibrillation

Objectives

To investigate the role and mechanism of MAPK14/AIFM2 pathway in Ang II-induced atrial fibrillation in rats.

Methods

A rat model of AF was established for in vivo experiments and HL-1 cells were treated with Ang II to develop an in vitro model. In addition, HL1 cells overexpressing AIFM2 (oeAIFM2) were constructed. SB203580 was used to inhibit the expression of MAPK14. The role of MAPK14 in Ang II-AF model was investigated by in vivo electrophysiological examination and molecular biology tests. The role of MAPK14 / AIFM2 pathway on AF induced by Ang II was explored in vitro.

Results

MAPK14 and AIFM2 were significantly up-regulated in AF induced by Ang II (all P < 0.05). In vivo experiments indicated that inhibition of MAPK14 down-regulated AIFM2, improved atrial electrical conduction, AF inducibility and durations, and alleviated the structural and functional damage of heart and mitochondria (all P < 0.05). Both in vivo and in vitro tests showed that the MAPK14/AIFM2 pathway prevented Ang II-induced AF via regulating mitophagy-dependent apoptosis.

Conclusions

Inhibition of the MAPK14/AIFM2 pathway improved Ang II-induced AF by inhibiting mitophagy-dependent apoptosis.
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来源期刊
CiteScore
10.70
自引率
0.00%
发文量
171
审稿时长
42 days
期刊介绍: The Journal of Molecular and Cellular Cardiology publishes work advancing knowledge of the mechanisms responsible for both normal and diseased cardiovascular function. To this end papers are published in all relevant areas. These include (but are not limited to): structural biology; genetics; proteomics; morphology; stem cells; molecular biology; metabolism; biophysics; bioengineering; computational modeling and systems analysis; electrophysiology; pharmacology and physiology. Papers are encouraged with both basic and translational approaches. The journal is directed not only to basic scientists but also to clinical cardiologists who wish to follow the rapidly advancing frontiers of basic knowledge of the heart and circulation.
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