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ANGPTL2 activity in cardiac pathologies accelerates heart failure by perturbing cardiac function and energy

Zhe Tian1,2, Keishi Miyata1,3, Tsuyoshi Kadomatsu1

  • 1Department of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University, Kumamoto 860-8556, Japan.

Nature Communications
|September 29, 2016
PubMed

Insights

ANGPTL2 protein promotes heart failure by disrupting cardiac function and energy metabolism. Suppressing ANGPTL2 offers a potential therapeutic strategy to prevent heart failure development.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Pathophysiology

Background:

  • Cardiac remodeling is a response to increased workload, which can become pathological and lead to heart failure.
  • The precise molecular mechanisms driving pathological cardiac remodeling remain incompletely understood.

Purpose of the Study:

  • To investigate the role of angiopoietin-like protein 2 (ANGPTL2) in cardiac remodeling and heart failure.
  • To explore ANGPTL2 as a potential therapeutic target for heart failure.

Main Methods:

  • Assessed ANGPTL2 expression in mouse models of physiological and pathological cardiac remodeling, and in human heart samples.
  • Utilized cardiac-specific ANGPTL2 overexpression and knockout mouse models.
  • Examined the effects of ANGPTL2 manipulation on cardiac function, AKT and SERCA2a signaling, and myocardial energy metabolism.
  • Investigated ANGPTL2 knockdown in a pressure overload-induced heart failure mouse model.

Main Results:

  • ANGPTL2 expression is elevated in pathological cardiac remodeling but decreased in physiological remodeling.
  • ANGPTL2 overexpression impairs cardiac function by inhibiting AKT and SERCA2a signaling and reducing energy metabolism.
  • ANGPTL2 deficiency enhances cardiac contractility and upregulates AKT-SERCA2a signaling and energy metabolism.
  • ANGPTL2 knockdown mitigates cardiac dysfunction in pressure overload-induced heart failure.

Conclusions:

  • ANGPTL2 plays a critical role in the development of pathological cardiac remodeling and heart failure.
  • Therapeutic suppression of ANGPTL2 may represent a novel strategy to prevent or treat heart failure.

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