Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 15, Issue 4, Pages 5304-5322Publisher
MDPI
DOI: 10.3390/ijms15045304
Keywords
myocardial infarction; mitochondrial dysfunction; fusion; fission; mitochondrial dynamics; aerobic interval training
Funding
- National Natural Science Foundation of China [30930105]
- Major International (Regional) Joint Research Project of National Natural Science Foundation of China [81120108002]
- Specialized Research Fund for the Doctoral Program of Higher Education [20130201130008]
- Natural Science Foundation of Shaanxi Province [2012JZ4001]
- CMB Distinguished Professorships Award [F510000/G16916404]
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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-1a); 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-1 alpha. 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-1 alpha 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-1 alpha expression.
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