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Related Concept Videos

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Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
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The development of the human heart, a crucial organ, commences from the mesoderm on the 18th or 19th day after fertilization. This process initiates in the cardiogenic area, a group of mesodermal cells at the embryo's head end, which evolves into elongated strands known as cardiogenic cords. These cords undergo a transformation to form hollow-centered endocardial tubes.
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Decrease of Pdzrn3 is required for heart maturation and protects against heart failure.

Mathieu Pernot1, Béatrice Jaspard-Vinassa1, Alice Abelanet1

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PDZRN3, an E3 ubiquitin ligase, regulates cardiomyocyte organization. Its dysregulation causes heart failure, but blocking PDZRN3 protects heart function, suggesting it as a therapeutic target.

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Area of Science:

  • Cardiology
  • Molecular Biology
  • Cell Biology

Background:

  • Heart failure involves cardiomyocyte (CM) alterations at cell contact sites.
  • Planar cell polarity (PCP) signaling is crucial for CM organization and cardiac function.
  • PDZRN3, an E3 ubiquitin ligase, is implicated in PCP signaling and tissue patterning.

Purpose of the Study:

  • To investigate the role of PDZRN3 in cardiomyocyte polarization and heart failure.
  • To determine if PDZRN3 is a potential therapeutic target for heart failure.

Main Methods:

  • Utilized mouse models with cardiomyocyte-specific PDZRN3 overexpression (OE) and knockout (KO).
  • Analyzed cardiac function, CM morphology, and expression of key signaling molecules (PKC ζ, c-Jun, β-catenin).
  • Examined the subcellular localization of intercalated disk proteins (Cx43, ZO1, Desmoglein 2).

Main Results:

  • Moderate CM PDZRN3 OE induced eccentric hypertrophy and heart failure.
  • CM-specific PDZRN3 KO completely protected against pressure-overload induced heart failure.
  • PDZRN3 signaling altered junction protein localization, impairing CM polarization.
  • PDZRN3 OE affected PKC ζ, c-Jun, and β-catenin levels, consistent with non-canonical Wnt signaling.

Conclusions:

  • PDZRN3 controls a genetic program vital for heart maturation and function.
  • Altered PDZRN3 levels disrupt CM organization and lead to heart failure.
  • PDZRN3 is a novel therapeutic target for preventing and treating heart failure.