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Follistatin-Like 1 Protects against Doxorubicin-Induced Cardiomyopathy through Upregulation of Nrf2

Yintao Zhao1, Jingjing Sun1, Wei Zhang2

  • 1Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.

Oxidative Medicine and Cellular Longevity
|August 25, 2020
PubMed

Insights

Follistatin-like 1 (FSTL1) protects against Doxorubicin- (DOX-) induced heart damage. This protein prevents cardiac injury and improves heart function by upregulating nuclear factor erythroid 2-related factor 2 (Nrf2).

Area of Science:

  • Cardiology
  • Molecular Biology
  • Pharmacology

Background:

  • Doxorubicin (DOX) chemotherapy can cause irreversible heart failure (cardiomyopathy) due to cardiomyocyte loss.
  • No effective treatments currently exist for DOX-induced cardiotoxicity.
  • Follistatin-like 1 (FSTL1) has shown protective effects against other forms of cardiac injury.

Purpose of the Study:

  • To investigate the potential of Follistatin-like 1 (FSTL1) in preventing Doxorubicin (DOX)-induced cardiotoxicity in a mouse model.
  • To elucidate the underlying molecular mechanisms of FSTL1's protective effects against DOX.

Main Methods:

  • Mice received a single dose of Doxorubicin (DOX) to induce acute cardiotoxicity.
  • Adeno-associated virus (AAV) system was used for cardiac overexpression of Follistatin-like 1 (FSTL1).
  • Cardiac function, oxidative stress, apoptosis, and gene expression (including Nrf2) were assessed.
  • Experiments were also conducted in Nrf2-deficient mice to confirm the mechanism.

Main Results:

  • Doxorubicin (DOX) administration reduced Follistatin-like 1 (FSTL1) expression in the heart.
  • FSTL1 overexpression attenuated DOX-induced cardiac injury, oxidative stress, and apoptosis, improving cardiac function.
  • FSTL1 improved cardiomyocyte contractility in vitro and upregulated nuclear factor (erythroid-derived 2)-like 2 (Nrf2) expression.
  • FSTL1's protective effects were abolished in Nrf2-deficient mice.

Conclusions:

  • Follistatin-like 1 (FSTL1) demonstrates significant protective effects against Doxorubicin (DOX)-induced cardiotoxicity in mice.
  • The cardioprotective mechanism of FSTL1 involves the upregulation of nuclear factor (erythroid-derived 2)-like 2 (Nrf2).

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