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Mitoquinone Prevents Cardiac Dysfunction by Normalizing Mitochondrial ROS and Calcium Handling in Acute Myocardial

Carolina Falcão Ximenes1, Pietra Zava Lorencini1, Carmen Castardeli1

  • 1Post-Graduate Program in Physiological Sciences, Federal University of Espírito Santo, Vitória, Espírito Santo, Brazil.

Acta Physiologica (Oxford, England)
|July 11, 2026
PubMed
Summary
This summary is machine-generated.

Mitochondrial oxidative stress contributes to heart dysfunction after myocardial infarction (MI). The antioxidant MitoQ improved cardiac function and reduced oxidative stress in rats, suggesting a promising therapeutic strategy for preventing heart failure (HF) post-MI.

Keywords:
mitochondriamyocardial contractilitymyocardial infarctionoxidative stressreactivity oxygen species

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Area of Science:

  • Cardiovascular Research
  • Mitochondrial Biology
  • Pharmacology

Background:

  • Acute myocardial infarction (MI) is a primary cause of heart failure (HF).
  • The specific role of mitochondrial reactive oxygen species (ROS) in early MI-induced cardiac dysfunction is not fully understood.
  • Mitochondrial dysfunction is increasingly recognized as a key factor in cardiovascular diseases.

Purpose of the Study:

  • To investigate the impact of MitoQ, a mitochondria-targeted antioxidant, on cardiac function following MI.
  • To determine if reducing mitochondrial ROS can mitigate early cardiac dysfunction after MI.
  • To explore the underlying mechanisms of MitoQ's effects on oxidative stress and cardiac performance.

Main Methods:

  • Male Wistar rats underwent MI or sham surgery and were treated with or without MitoQ (8 mg/kg/day orally for 7 days).
  • Evaluated hemodynamic parameters, infarct size, papillary muscle contractility, cardiomyocyte mechanics, and intracellular calcium (Ca2+) transients.
  • Assessed total and mitochondrial superoxide production using DHE and MitoSOX staining, and measured NOX1, NOX2, SOD1, and catalase expression.

Main Results:

  • MI induced cardiac dysfunction, cardiomyocyte hypertrophy, and increased mitochondrial ROS production.
  • MitoQ treatment significantly improved hemodynamic parameters, restored papillary muscle contractility, and attenuated cardiomyocyte hypertrophy and Ca2+ transient alterations.
  • MitoQ markedly reduced mitochondrial superoxide production and selectively decreased NOX1 expression.

Conclusions:

  • Mitochondrial oxidative stress plays a critical role in acute myocardial infarction-induced cardiac dysfunction.
  • Targeting mitochondria with antioxidants like MitoQ is a promising therapeutic strategy for preventing post-MI heart failure.
  • This study highlights the potential of MitoQ in managing cardiovascular diseases and improving outcomes after MI.