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

Reza Ghahremani, Arsalan Damirchi, Iraj Salehi, Alireza Komaki, Fabio Esposito

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Aims: 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. Main methods: 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. Key findings: 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). Significance: Exercise-induced regulation of mitochondrial fusion and fission, leading to improvement of mitochondrial dynamics seems to be involved in the cardioprotection against IR injuries.

Original languageEnglish
Pages (from-to)102-108
Number of pages7
JournalLife Sciences
Volume213
DOIs
Publication statusPublished - Nov 15 2018

Fingerprint

Mitochondrial Dynamics
Reperfusion Injury
Exercise
Rats
Dynamin II
Fusion reactions
Dynamins
Wounds and Injuries
Exercise equipment
Silk
Analysis of variance (ANOVA)
Gene expression
Thoracotomy
Statistical methods
Proteins
Sutures
Reperfusion
Wistar Rats
Coronary Vessels
Analysis of Variance

Keywords

  • Aerobic training
  • Cardioprotection
  • Ischemia-reperfusion
  • Mitochondrial dynamics

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Pharmacology, Toxicology and Pharmaceutics(all)

Cite this

Mitochondrial dynamics as an underlying mechanism involved in aerobic exercise training-induced cardioprotection against ischemia-reperfusion injury. / Ghahremani, Reza; Damirchi, Arsalan; Salehi, Iraj; Komaki, Alireza; Esposito, Fabio.

In: Life Sciences, Vol. 213, 15.11.2018, p. 102-108.

Research output: Contribution to journalArticle

Ghahremani, Reza ; Damirchi, Arsalan ; Salehi, Iraj ; Komaki, Alireza ; Esposito, Fabio. / Mitochondrial dynamics as an underlying mechanism involved in aerobic exercise training-induced cardioprotection against ischemia-reperfusion injury. In: Life Sciences. 2018 ; Vol. 213. pp. 102-108.
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AU - Esposito, Fabio

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AB - Aims: 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. Main methods: 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. Key findings: 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). Significance: Exercise-induced regulation of mitochondrial fusion and fission, leading to improvement of mitochondrial dynamics seems to be involved in the cardioprotection against IR injuries.

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