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Related Concept Videos

Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

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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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Cardiomyopathy V: Interprofessional Care01:29

Cardiomyopathy V: Interprofessional Care

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Managing cardiomyopathy involves addressing underlying or precipitating causes, treating heart failure with medications, and implementing dietary changes and a balanced exercise and rest regimen.Lifestyle ModificationsCardiomyopathy patients should adopt a low-sodium diet to reduce fluid retention and manage heart failure. A personalized exercise and rest plan helps maintain physical fitness without overstraining the heart. Avoiding alcohol and tobacco is essential to prevent further damage to...
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Cardiomyopathy I: Introduction and Classification01:25

Cardiomyopathy I: Introduction and Classification

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Cardiomyopathy, or CMP, is a group of diseases affecting the myocardial structure, impairing its ability to pump blood effectively. This condition can lead to arrhythmias, heart failure, or sudden cardiac death.Cardiomyopathies are classified into primary and secondary categories:Primary Cardiomyopathy refers to conditions involving only the heart muscle that are often idiopathic (of unknown cause) or genetic. They primarily affect the myocardium without the involvement of other systemic...
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Cardiomyopathy II: Dilated Cardiomyopathy01:30

Cardiomyopathy II: Dilated Cardiomyopathy

480
Dilated cardiomyopathy, or DCM, is a progressive myocardial disorder characterized by ventricular chamber dilation and contractile dysfunction.EtiologyVarious factors can cause DCM, including hypertension and heavy alcohol intake, which contribute to the weakening and enlargement of the heart muscle. Viral infections, such as Coxsackievirus B, adenoviruses, and influenza, can lead to DCM by causing inflammation and damage to heart tissue. Certain chemotherapeutic agents, including daunorubicin,...
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Related Experiment Video

Updated: Jan 17, 2026

Technique of Minimally Invasive Transverse Aortic Constriction in Mice for Induction of Left Ventricular Hypertrophy
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Targeting Cardiomyocyte PCNA and POLD1 Prevents Pathologic Myocardial Hypertrophy.

Soumojit Pal1, Michael S Glennon1, Benjamin R Nixon1

  • 1Division of Cardiology, Department of Medicine and Pittsburgh Heart, Lung, Blood, and Vascular Medicine Institute, University of Pittsburgh School of Medicine and University of Pittsburgh Medical Center, PA (S.P., M.S.G., B.R.N., E.J.C., P.S., C.M.K., M.B.G., C.J.W., L.G., N.G.C., D.B., J.H.K., J.R.B.).

Circulation Research
|September 15, 2025
PubMed
Summary
This summary is machine-generated.

Targeting DNA synthesis pathways, specifically PCNA-POLD1, can reduce pathological cardiomyocyte growth and hypertrophy. The protein p21 acts as a negative regulator, offering therapeutic potential for heart conditions.

Keywords:
cardiomyopathy, hypertrophicdisease models, animalendoreduplicationheart failurehypertrophymyocytes, cardiacpolyploidy

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Last Updated: Jan 17, 2026

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Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Cell Cycle Regulation

Background:

  • Pathological cardiomyocyte growth involves cell cycle regulatory pathways.
  • The role of DNA synthesis in cardiomyocyte hypertrophy was previously unclear.
  • Increased DNA synthesis and endoreplication were observed in a mouse model of hypertrophic cardiomyopathy.

Purpose of the Study:

  • To investigate the role of DNA synthesis pathways in cardiomyocyte hypertrophy.
  • To determine if targeting cardiomyocyte endoreplication can reduce pathological myocardial hypertrophy.
  • To explore the regulatory function of p21 in this process.

Main Methods:

  • Utilized murine models of hypertrophic cardiomyopathy (Mybpc3-/-, Myh6R404Q) and pressure overload.
  • Manipulated p21 (cyclin dependent kinase inhibitor 1) levels in vivo.
  • Assessed cardiomyocyte endoreplication via flow cytometry and immunohistochemistry; employed proteomics and human iPSC-derived cardiomyocytes.

Main Results:

  • p21 levels peaked during early hypertrophic growth.
  • p21 expression negatively correlated with cardiomyocyte endoreplication and hypertrophy.
  • p21 inhibited PCNA (proliferating cell nuclear antigen) binding to POLD1 (DNA polymerase delta 1), preventing DNA synthesis and hypertrophy.
  • Overexpression of p21 reduced left ventricular hypertrophy and improved diastolic function.

Conclusions:

  • PCNA-POLD1-mediated cardiomyocyte endoreplication drives hypertrophic growth.
  • p21 negatively regulates this endoreplication pathway.
  • Targeting these pathways holds therapeutic potential for pathological myocardial hypertrophy.