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A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
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A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo

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Doxorubicin-induced cardiomyocyte apoptosis: Role of mitofusin 2

Han Tang1, Aibin Tao2, Jia Song1

  • 1Division of Cardiology, Department of Medicine, The Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu, China.

The International Journal of Biochemistry & Cell Biology
|May 10, 2017
PubMed
Abstract

Insights

Doxorubicin (DOX) treatment decreases Mitofusin 2 (Mfn2) in heart cells, increasing mitochondrial damage and apoptosis. Restoring Mfn2 levels protects against DOX-induced cardiotoxicity.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Toxicology

Background:

  • Doxorubicin (DOX) is a vital anti-cancer drug.
  • DOX causes cardiotoxicity, leading to heart failure via unknown mechanisms.
  • Mitofusin 2 (Mfn2) regulates mitochondrial fusion and is crucial for mitochondrial health.

Purpose of the Study:

  • Investigate the role of Mfn2 in Doxorubicin-induced cardiomyocyte apoptosis.
  • Determine if Mfn2 levels influence mitochondrial dysfunction during DOX treatment.

Main Methods:

  • Neonatal rat cardiomyocytes were exposed to DOX.
  • Mfn2 expression, mitochondrial fission, reactive oxygen species (ROS) production, and apoptosis were measured.
  • Mfn2 levels were manipulated to assess its protective effects.

Main Results:

  • DOX exposure increased cardiomyocyte oxidative stress and apoptosis.
  • DOX reduced Mfn2 levels, correlating with increased mitochondrial fission and ROS.
  • Elevated Mfn2 attenuated DOX-induced mitochondrial fission and ROS production.
  • Increased Mfn2 or antioxidant treatment protected cardiomyocytes from DOX-induced apoptosis.

Conclusions:

  • DOX diminishes Mfn2 expression in cardiomyocytes.
  • Reduced Mfn2 exacerbates mitochondrial fission and ROS production, causing apoptosis.
  • Mfn2 plays a protective role against DOX cardiotoxicity.
Keywords:
Cardiomyocyte apoptosisDoxorubicinMitochondrial reactive oxygen speciesMitofusin 2

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