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Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
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Hippo pathway deficiency reverses systolic heart failure after infarction.

John P Leach1, Todd Heallen2, Min Zhang1,3

  • 1Department of Molecular Physiology and Biophysics, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA.

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|October 5, 2017
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Summary
This summary is machine-generated.

Deleting the Hippo pathway component Salvador (Salv) in mice with heart failure promotes repair. This involves increased vascularity, reduced fibrosis, and improved heart function, highlighting a previously unrecognized reparative capacity.

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Area of Science:

  • Cardiovascular Biology
  • Regenerative Medicine
  • Molecular Cardiology

Background:

  • Mammalian organs have limited regenerative capacity, with the heart being particularly susceptible to failure after injury.
  • Heart failure, often resulting in mortality, is associated with upregulated Hippo pathway signaling, which inhibits adult cardiomyocyte proliferation.
  • The Hippo pathway acts as a critical regulator of organ size and regeneration.

Purpose of the Study:

  • To investigate the role of the Hippo pathway, specifically the Salvador (Salv) component, in the context of established ischemic heart failure.
  • To determine if modulating the Hippo pathway can induce a reparative genetic program in cardiomyocytes and improve cardiac function.
  • To explore the potential of gene therapy targeting the Hippo pathway for treating heart failure.

Main Methods:

  • Utilized a mouse model of established ischemic heart failure following myocardial infarction.
  • Deleted the Hippo pathway component Salvador (Salv) in cardiomyocytes.
  • Employed translating ribosomal affinity purification to analyze cardiomyocyte-specific messenger RNA.
  • Conducted genetic studies to assess the role of specific genes, such as Park2, in heart repair.
  • Administered gene therapy using a virus encoding Salv short hairpin RNA.

Main Results:

  • Deletion of Salv in failing mouse hearts initiated a reparative program, characterized by increased scar border vascularity and reduced fibrosis.
  • Hippo-deficient cardiomyocytes exhibited increased expression of proliferative and stress response genes, including the mitochondrial quality control gene Park2.
  • Genetic ablation of Park2 impaired heart repair, indicating its essential role in myocardial regeneration.
  • Gene therapy with Salv short hairpin RNA improved cardiac function, whether delivered during infarct or after heart failure was established.
  • The study revealed enhanced pumping function in treated mice compared to controls.

Conclusions:

  • The Hippo pathway is a key regulator of cardiomyocyte proliferation and regeneration, and its inhibition can promote cardiac repair.
  • Park2-mediated mitochondrial quality control is crucial for the regenerative capacity of the myocardium.
  • Targeting the Hippo pathway, for example, via gene therapy with Salv short hairpin RNA, offers a promising therapeutic strategy for heart failure.
  • The failing heart possesses a latent reparative potential that can be unlocked by modulating specific molecular pathways, extending beyond simple cardiomyocyte renewal.