Aerobic Interval Training Attenuates Mitochondrial Dysfunction in Rats Post-Myocardial Infarction: Roles of Mitochondrial Network Dynamics

International Journal of Molecular Sciences

Hong-Ke Jiang¹  You-Hua Wang¹  Lei Sun¹  Xi He¹  Mei Zhao¹  Zhi-Hui Feng²  Xiao-Jiang Yu¹ 

[1]Department of Pharmacology, College of Medicine, Xi’an Jiaotong University, Xi’an 710061, China

[2] E-Mails:

[3]Center for Mitochondrial Biology and Medicine, Key Laboratory of Biomedical Information Engineering of the Ministry of Education, School of Life Science and Technology, Frontier Institute of Science and Technology, Xi’an Jiaotong University, Xi’an 710049, China

[4] E-Mail:

关键词: myocardial infarction;    mitochondrial dysfunction;    fusion;    fission;    mitochondrial dynamics;    aerobic interval training;   

DOI  :  10.3390/ijms15045304

来源: mdpi

【 摘 要 】

Aerobic interval training (AIT) can favorably affect cardiovascular diseases. However, the effects of AIT on post-myocardial infarction (MI)—associated mitochondrial dysfunctions remain unclear. In this study, we investigated the protective effects of AIT on myocardial mitochondria in post-MI rats by focusing on mitochondrial dynamics (fusion and fission). Mitochondrial respiratory functions (as measured by the respiratory control ratio (RCR) and the ratio of ADP to oxygen consumption (P/O)); complex activities; dynamic proteins (mitofusin (mfn) 1/2, type 1 optic atrophy (OPA1) and dynamin-related protein1 (DRP1)); nuclear peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α); and the oxidative signaling of extracellular signal-regulated kinase (ERK) 1/2, c-Jun NH₂-terminal protein kinase (JNK) and P53 were observed. Post-MI rats exhibited mitochondrial dysfunction and adverse mitochondrial network dynamics (reduced fusion and increased fission), which was associated with activated ERK1/2-JNK-P53 signaling and decreased nuclear PGC-1α. After AIT, MI-associated mitochondrial dysfunction was improved (elevated RCR and P/O and enhanced complex I, III and IV activities); in addition, increased fusion (mfn2 and OPA1), decreased fission (DRP1), elevated nuclear PGC-1α and inactivation of the ERK1/2-JNK-P53 signaling were observed. These data demonstrate that AIT may restore the post-MI mitochondrial function by inhibiting dynamics pathological remodeling, which may be associated with inactivation of ERK1/2-JNK-P53 signaling and increase in nuclear PGC-1α expression.

【 授权许可】

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© 2014 by the authors; licensee MDPI, Basel, Switzerland