Exercise Training Enhances Myocardial Mitophagy and Improves Cardiac Function via Irisin/FNDC5-PINK1/Parkin Pathway in MI Mice

Myocardial infarction is the major cause of death in cardiovascular disease. In vitro and in vivo models are used to find the exercise mode which has the most significant effect on myocardial irisin/FNDC5 expression and illuminate the cardioprotective role and mechanisms of exercise-activated myocar...

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Main Authors: Hangzhuo Li, Shuguang Qin, Qiaoqin Liang, Yue Xi, Wenyan Bo, Mengxin Cai, Zhenjun Tian
Format: Article
Language:English
Published: MDPI AG 2021-06-01
Series:Biomedicines
Subjects:
Online Access:https://www.mdpi.com/2227-9059/9/6/701
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author Hangzhuo Li
Shuguang Qin
Qiaoqin Liang
Yue Xi
Wenyan Bo
Mengxin Cai
Zhenjun Tian
author_facet Hangzhuo Li
Shuguang Qin
Qiaoqin Liang
Yue Xi
Wenyan Bo
Mengxin Cai
Zhenjun Tian
author_sort Hangzhuo Li
collection DOAJ
description Myocardial infarction is the major cause of death in cardiovascular disease. In vitro and in vivo models are used to find the exercise mode which has the most significant effect on myocardial irisin/FNDC5 expression and illuminate the cardioprotective role and mechanisms of exercise-activated myocardial irisin/FNDC5-PINK1/Parkin-mediated mitophagy in myocardial infarction. The results indicated that expression of irisin/FNDC5 in myocardium could be up-regulated by different types of exercise and skeletal muscle electrical stimulation, which then promotes mitophagy and improves cardiac function and the effect of resistance exercise. Resistance exercise can improve cardiac function by activating the irisin/FNDC5-PINK1/Parkin-LC3/P62 pathway, regulating mitophagy and inhibiting oxidative stress. OPA1 may play an important role in the improvement of cardiac function and mitophagy pathway in myocardial infarction mice by irisin-mediated resistance exercise. Resistance exercise is expected to become an effective therapeutic way to promote myocardial infarction rehabilitation.
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spelling doaj.art-f78d10d18d0849f993ed3ab407e0630c2023-11-22T01:01:26ZengMDPI AGBiomedicines2227-90592021-06-019670110.3390/biomedicines9060701Exercise Training Enhances Myocardial Mitophagy and Improves Cardiac Function via Irisin/FNDC5-PINK1/Parkin Pathway in MI MiceHangzhuo Li0Shuguang Qin1Qiaoqin Liang2Yue Xi3Wenyan Bo4Mengxin Cai5Zhenjun Tian6Institute of Sports and Exercise Biology, School of Physical Education, Shaanxi Normal University, Xi’an 710119, ChinaInstitute of Sports and Exercise Biology, School of Physical Education, Shaanxi Normal University, Xi’an 710119, ChinaInstitute of Sports and Exercise Biology, School of Physical Education, Shaanxi Normal University, Xi’an 710119, ChinaInstitute of Sports and Exercise Biology, School of Physical Education, Shaanxi Normal University, Xi’an 710119, ChinaInstitute of Sports and Exercise Biology, School of Physical Education, Shaanxi Normal University, Xi’an 710119, ChinaInstitute of Sports and Exercise Biology, School of Physical Education, Shaanxi Normal University, Xi’an 710119, ChinaInstitute of Sports and Exercise Biology, School of Physical Education, Shaanxi Normal University, Xi’an 710119, ChinaMyocardial infarction is the major cause of death in cardiovascular disease. In vitro and in vivo models are used to find the exercise mode which has the most significant effect on myocardial irisin/FNDC5 expression and illuminate the cardioprotective role and mechanisms of exercise-activated myocardial irisin/FNDC5-PINK1/Parkin-mediated mitophagy in myocardial infarction. The results indicated that expression of irisin/FNDC5 in myocardium could be up-regulated by different types of exercise and skeletal muscle electrical stimulation, which then promotes mitophagy and improves cardiac function and the effect of resistance exercise. Resistance exercise can improve cardiac function by activating the irisin/FNDC5-PINK1/Parkin-LC3/P62 pathway, regulating mitophagy and inhibiting oxidative stress. OPA1 may play an important role in the improvement of cardiac function and mitophagy pathway in myocardial infarction mice by irisin-mediated resistance exercise. Resistance exercise is expected to become an effective therapeutic way to promote myocardial infarction rehabilitation.https://www.mdpi.com/2227-9059/9/6/701exercise trainingmyocardial infarctionmicemitophagyirisin
spellingShingle Hangzhuo Li
Shuguang Qin
Qiaoqin Liang
Yue Xi
Wenyan Bo
Mengxin Cai
Zhenjun Tian
Exercise Training Enhances Myocardial Mitophagy and Improves Cardiac Function via Irisin/FNDC5-PINK1/Parkin Pathway in MI Mice
Biomedicines
exercise training
myocardial infarction
mice
mitophagy
irisin
title Exercise Training Enhances Myocardial Mitophagy and Improves Cardiac Function via Irisin/FNDC5-PINK1/Parkin Pathway in MI Mice
title_full Exercise Training Enhances Myocardial Mitophagy and Improves Cardiac Function via Irisin/FNDC5-PINK1/Parkin Pathway in MI Mice
title_fullStr Exercise Training Enhances Myocardial Mitophagy and Improves Cardiac Function via Irisin/FNDC5-PINK1/Parkin Pathway in MI Mice
title_full_unstemmed Exercise Training Enhances Myocardial Mitophagy and Improves Cardiac Function via Irisin/FNDC5-PINK1/Parkin Pathway in MI Mice
title_short Exercise Training Enhances Myocardial Mitophagy and Improves Cardiac Function via Irisin/FNDC5-PINK1/Parkin Pathway in MI Mice
title_sort exercise training enhances myocardial mitophagy and improves cardiac function via irisin fndc5 pink1 parkin pathway in mi mice
topic exercise training
myocardial infarction
mice
mitophagy
irisin
url https://www.mdpi.com/2227-9059/9/6/701
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