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A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
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miR-451 Silencing Inhibited Doxorubicin Exposure-Induced Cardiotoxicity in Mice

Jun Li1, Weiguo Wan1, Tao Chen1

  • 1Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China.

Biomed Research International
|July 30, 2019
PubMed

Insights

Inhibiting microRNA-451 (miR-451) protected against doxorubicin-induced heart damage by reducing oxidative stress and cell death. This protection involved activating the AMPK signaling pathway in cardiomyocytes.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Biochemistry

Background:

  • Doxorubicin (Dox) causes cardiac injury through oxidative stress and cardiomyocyte apoptosis.
  • MicroRNA-451 (miR-451) is expressed in cardiomyocytes, but its role in Dox-induced cardiotoxicity is unknown.

Purpose of the Study:

  • To investigate the protective effect of miR-451 inhibition against Dox-induced cardiotoxicity in a mouse model.

Main Methods:

  • A Dox-induced cardiotoxicity mouse model was established.
  • miR-451 expression was manipulated using a miR-451 inhibitor.
  • Cardiac function, oxidative stress, and apoptosis were evaluated.
  • Expression of calcium binding protein 39 (Cab39) and the AMPK signaling pathway were assessed.

Main Results:

  • Dox treatment increased miR-451 levels in mice and cardiomyocytes.
  • miR-451 inhibition attenuated Dox-induced wasting, heart atrophy, and cardiac injury.
  • Inhibition of miR-451 improved cardiac and cardiomyocyte function, reduced oxidative stress, and decreased apoptosis.
  • miR-451 inhibition upregulated Cab39 and activated the AMPK pathway, which was crucial for cardioprotection.

Conclusions:

  • miR-451 inhibition confers protection against doxorubicin-induced cardiotoxicity.
  • This protective effect is mediated through the activation of the AMPK signaling pathway.

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