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Related Concept Videos

Heart Failure II: Pathophysiology01:29

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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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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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Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The...
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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

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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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Related Experiment Video

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PDE1C deficiency antagonizes pathological cardiac remodeling and dysfunction.

Walter E Knight1,2, Si Chen1,2, Yishuai Zhang1

  • 1Aab Cardiovascular Research Institute, Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY 14641.

Proceedings of the National Academy of Sciences of the United States of America
|October 30, 2016
PubMed
Summary

Cyclic nucleotide phosphodiesterase 1C (PDE1C) plays a key role in pathological cardiac remodeling and dysfunction. Inhibiting PDE1C in failing hearts may offer significant therapeutic benefits for heart conditions.

Keywords:
cardiac remodelingcyclic nucleotideheart failurephosphodiesterase

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Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Enzyme Function

Background:

  • Cyclic nucleotide phosphodiesterase 1C (PDE1C) is a major phosphodiesterase in the human heart, but its specific role in cardiac function is not well understood.
  • Cardiac remodeling and dysfunction are significant contributors to heart failure.
  • Understanding the molecular mechanisms underlying cardiac remodeling is crucial for developing effective therapies.

Purpose of the Study:

  • To investigate the expression, regulation, function, and mechanisms of PDE1C in the context of cardiac remodeling and dysfunction.
  • To determine the role of PDE1C in cardiac myocyte death, hypertrophy, and fibroblast activation.
  • To evaluate the therapeutic potential of targeting PDE1C in pathological cardiac conditions.

Main Methods:

  • Utilized genetic (PDE1C-knockout mice) and pharmacological inhibition approaches.
  • Examined PDE1C expression in mouse and human failing hearts and isolated cardiac myocytes.
  • Assessed the impact of PDE1C deficiency/inhibition on cardiac myocyte apoptosis and hypertrophy.
  • Investigated the effects on cardiac fibroblast activation and in vivo cardiac remodeling following transverse aortic constriction.

Main Results:

  • PDE1C expression is upregulated in failing hearts and localized to cardiac myocytes.
  • PDE1C deficiency or inhibition attenuated cardiac myocyte death, apoptosis (via cAMP/PKA and PI3K/AKT pathways), and hypertrophy (via PKA).
  • Conditioned media from PDE1C-deficient myocytes reduced TGF-β-stimulated fibroblast activation, indicating myocyte-fibroblast crosstalk modulation.
  • PDE1C knockout mice showed significantly attenuated cardiac remodeling and dysfunction in response to pressure overload.

Conclusions:

  • PDE1C activation is a causative factor in pathological cardiac remodeling and dysfunction.
  • Targeting PDE1C may represent a promising therapeutic strategy for treating heart failure.
  • The high expression of PDE1C in the human heart underscores its potential as a drug target.