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The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
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Updated: Mar 2, 2026

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
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Exercise and Doxorubicin Treatment Modulate Cardiac Mitochondrial Quality Control Signaling.

I Marques-Aleixo1, E Santos-Alves2,3, J R Torrella3

  • 1CIAFEL - Research Centre in Physical Activity, Health and Leisure, Faculty of Sport, University of Porto, Rua Dr. Plácido Costa 91, 4200-450, Porto, Portugal. inesmaleixo@hotmail.com.

Cardiovascular Toxicology
|May 25, 2017
PubMed
Summary
This summary is machine-generated.

Exercise training, including treadmill and free wheel activity, protects heart mitochondria from Doxorubicin-induced damage by preventing apoptosis and regulating mitochondrial dynamics and autophagy.

Keywords:
AdriamycinCardiac cell deathChronic exerciseHeart mitochondriaMitochondrial quality control

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Area of Science:

  • Cardiovascular Physiology
  • Mitochondrial Biology
  • Exercise Science

Background:

  • Sub-chronic Doxorubicin (DOX) treatment can induce cardiotoxicity by affecting mitochondrial quality control, remodeling, and death pathways.
  • The protective effects of exercise against DOX-induced mitochondrial dysfunction are not well understood.

Purpose of the Study:

  • To investigate the cross-tolerance effects of two chronic exercise models (treadmill training and voluntary free wheel activity) on heart mitochondrial mechanisms during sub-chronic DOX treatment.
  • To analyze the impact of exercise on mitochondrial permeability transition pore (mPTP) susceptibility, apoptotic and autophagic signaling, and mitochondrial dynamics.

Main Methods:

  • Male Sprague-Dawley rats were subjected to 12 weeks of treadmill training (TM) or voluntary free wheel activity (FW) concurrently with 7 weeks of sub-chronic DOX treatment (2 mg/kg/week).
  • Measurements included caspase activity, protein expression of apoptosis markers (Bax, Bcl2), mPTP components (CypD, ANT), mitochondrial dynamics proteins (Mfn1, Mfn2, OPA1, DRP1), and autophagy markers (LC3, Beclin1, Pink1, Parkin, p62).

Main Results:

  • DOX treatment increased mPTP susceptibility, apoptotic signaling (caspase 3, 8, 9; Bax/Bcl2 ratio), and altered mitochondrial dynamics by decreasing fusion proteins (Mfn1, Mfn2, OPA1) and increasing fission protein (DRP1).
  • DOX also activated auto(mito)phagy signaling.
  • Both TM and FW exercise interventions prevented DOX-induced increases in mPTP susceptibility, apoptosis, and normalized mitochondrial dynamics and auto(mito)phagy signaling.

Conclusions:

  • Chronic exercise, whether endurance or voluntary, confers cross-tolerance against DOX-induced cardiotoxicity at the mitochondrial level.
  • Exercise effectively limits cardiac mitochondrial-driven apoptosis and regulates mitochondrial dynamics and autophagy in DOX-treated animals.