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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MDPI AG
2021-06-01
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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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language | English |
last_indexed | 2024-03-10T10:14:12Z |
publishDate | 2021-06-01 |
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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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