Mitochondrial dynamics as an underlying mechanism involved in aerobic exercise training-induced cardioprotection against ischemia-reperfusion injury

Ischemia-reperfusion injury is one of the most common cardiac disorders leading to irreversible heart damage. Many underlying mechanisms seem to be involved, among which mitochondrial dysfunction. Since physical training has a beneficial effect on mitochondrial dynamics (fusion and fission), it may...

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Vydané v:Life sciences (1973) Ročník 213; s. 102 - 108
Hlavní autori: Ghahremani, Reza, Damirchi, Arsalan, Salehi, Iraj, Komaki, Alireza, Esposito, Fabio
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: Netherlands Elsevier Inc 15.11.2018
Elsevier BV
Predmet:
Aerobic training
Aerobics
analysis of variance
Animals
Cardioprotection
cardioprotective effect
Cardiovascular system
Coronary artery
coronary vessels
Coronary Vessels - metabolism
Dynamics
Dynamin
Dynamins - metabolism
exercise
Exercise physiology
Fission
Gene expression
Heart
Heart - physiopathology
heart diseases
infarction
Injuries
Ischemia
Ischemia-reperfusion
laboratory animals
Male
males
Membrane Proteins - metabolism
Mitochondria
Mitochondria - drug effects
Mitochondria - physiology
Mitochondrial dynamics
Mitochondrial Dynamics - physiology
Mitochondrial Proteins - metabolism
Myocardial Infarction - physiopathology
Myocardial Reperfusion Injury - metabolism
Physical Conditioning, Animal - physiology
Physical training
Polymerase chain reaction
Proteins
Rats
Rats, Wistar
Reperfusion
Reperfusion Injury - prevention & control
Reperfusion Injury - therapy
reverse transcriptase polymerase chain reaction
Silk
staining
Statistical analysis
surgery
Triphenyltetrazolium chloride
Variance analysis
Ischemia-reperfusion
Cardioprotection
Mitochondrial dynamics
Aerobic training
ISSN:0024-3205, 1879-0631, 1879-0631
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Shrnutí:Ischemia-reperfusion injury is one of the most common cardiac disorders leading to irreversible heart damage. Many underlying mechanisms seem to be involved, among which mitochondrial dysfunction. Since physical training has a beneficial effect on mitochondrial dynamics (fusion and fission), it may have a cardioprotective effect against IR injury also via mitochondrial pathways. This study investigates the protective role of aerobic training against cardiac IR injury and the mitochondrial dynamics as a possible mechanism. Thirty-two male Wistar rats (8-week old) were divided into a control, sham, control + IR, and training + IR groups (8 rats each). Training group was exercised aerobically on a treadmill for 8 weeks (5 days/week). After 8 weeks, anesthetized rats underwent a left thoracotomy (sham, control + IR, and training + IR groups) to access the left anterior descending coronary artery, which was occluded by a silk suture for 30 min and released for 90 min of reperfusion (IR groups). Triphenyltetrazolium chloride staining was used to determine the infarct size. The gene expression of mitofusin 1 (Mfn1), mitofusin 2 (Mfn2), and dynamin-related protein 1 (Drp1) was evaluated by RT-PCR. A one-way ANOVA was used for statistical analysis with the significance level set at P ≤ 0.05. Cardiac infarct size was smaller In training + IR group (20.24 ± 5.7%) than in control + IR (35.9 ± 2.3%; P ≤ 0.05). Training + IR showed higher expression of Mfn1 and Mfn2 (P ≤ 0.05). Conversely, Drp1 expression was lower after training (P ≤ 0.05). Exercise-induced regulation of mitochondrial fusion and fission, leading to improvement of mitochondrial dynamics seems to be involved in the cardioprotection against IR injuries.
Bibliografia:ObjectType-Article-1
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ISSN:0024-3205
1879-0631
1879-0631
DOI:10.1016/j.lfs.2018.10.035