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The regulation of heart rate is a complex process controlled by the autonomic nervous system (ANS), hormonal influences, and intrinsic cardiac mechanisms. The ANS has two main components: the sympathetic nervous system (SNS) and the parasympathetic nervous system (PNS).
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The regulation of the cardiovascular system allows the body to adapt to various demands and maintain homeostasis.
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Cardiomyopathy IV: Restrictive Cardiomyopathy01:29

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Restrictive cardiomyopathy (RCM) is a rare heart muscle disease characterized by impaired ventricular filling due to stiffened ventricular walls, leading to significant diastolic dysfunction.EtiologyRestrictive cardiomyopathy can arise from both inherited and acquired diseases, many of which are systemic. It is categorized into four main types: infiltrative, storage, non-infiltrative, and endomyocardial diseases.Infiltrative diseases, such as amyloidosis, lead to RCM by depositing amyloid...
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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 II: Dilated Cardiomyopathy01:30

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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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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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Related Experiment Video

Updated: Nov 11, 2025

En Face Endocardial Cushion Preparation for Planar Morphogenesis Analysis in Mouse Embryos
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Creld1 regulates myocardial development and function.

Vera Beckert1, Sebastian Rassmann1, Amir Hossein Kayvanjoo2

  • 1Institute of Innate Immunity, Biophysical Imaging, Medical Faculty, University of Bonn, 53127 Bonn, Germany.

Journal of Molecular and Cellular Cardiology
|March 28, 2021
PubMed
Summary
This summary is machine-generated.

Cysteine-Rich with EGF-Like Domains 1 (CRELD1) is crucial for heart development. Myocardial CRELD1 deficiency impairs cardiac maturation and function, leading to postnatal lethality in mice.

Keywords:
Creld1ECMHeart developmentNotchTrabeculation

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Area of Science:

  • Cardiovascular Biology
  • Developmental Biology
  • Genetics

Background:

  • Cysteine-Rich with EGF-Like Domains 1 (CRELD1) is a known risk gene for human atrioventricular septal defects.
  • Previous studies in mouse models highlighted CRELD1's essential role in embryonic heart development, particularly septum and valve formation.
  • Global CRELD1 knockout leads to embryonic lethality, preventing investigation of its later-stage functions.

Purpose of the Study:

  • To investigate the cell type-specific functions of CRELD1 during peri- and postnatal heart development.
  • To elucidate the role of CRELD1 in endocardial and myocardial compartments.
  • To understand the molecular mechanisms underlying CRELD1's contribution to cardiac maturation and function.

Main Methods:

  • Generation of conditional CRELD1 knockout mouse models: endocardial-specific (KO Tie2) and myocardial-specific (KO MyHC).
  • Comprehensive cardiac phenotyping, including histology and immunohistochemistry.
  • Molecular analyses using RNA-sequencing and flow cytometry to assess signaling pathways and cellular changes.

Main Results:

  • CRELD1 function within the endocardium is dispensable for heart development.
  • Myocardial deletion of CRELD1 (KO MyHC) results in significant extracellular matrix remodeling and impaired trabeculation.
  • KO MyHC mice exhibit myocardial hypoplasia, leading to early postnatal lethality, mediated by Notch1 signaling pathway modulation.

Conclusions:

  • CRELD1 plays a dual role in heart development, essential for early septa/valve formation and later cardiac maturation.
  • Myocardial CRELD1 is critical for postnatal cardiac development, function, and survival.
  • These findings underscore CRELD1's vital importance in mammalian heart development and function throughout different life stages.