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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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Mitral Valve Stenosis (MVS) is a heart condition where the mitral valve narrows, impeding blood circulation from the left atrium to the left ventricle. The etiology and pathophysiology of this condition are multifaceted, leading to a cascade of cardiovascular complications.Causes of Mitral Valve StenosisRheumatic Heart Disease: It is the main cause of mitral valve stenosis, particularly in developing nations. This condition arises from rheumatic fever, an inflammatory illness resulting from...
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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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Mitral regurgitation is characterized by the backward circulation of blood from the left ventricle to the left atrium during systole, a phase of the cardiac cycle when the heart contracts and pumps blood out of the chambers. This abnormal flow occurs primarily due to the dysfunction of the mitral valve or its supporting structures, which include the mitral leaflets, chordae tendineae, annulus, and papillary muscles.Etiology and Mechanisms:Primary Mitral Regurgitation: This type arises from...
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Intrinsic Endocardial Defects Contribute to Hypoplastic Left Heart Syndrome.

Yifei Miao1, Lei Tian2, Marcy Martin3

  • 1Department of Pediatrics, Division of Pediatric Cardiology, Stanford School of Medicine, Stanford, CA 94305, USA; Vera Moulton Wall Center for Pulmonary Vascular Disease, Stanford School of Medicine, Stanford, CA 94305, USA; Stanford Cardiovascular Institute, Stanford School of Medicine, Stanford, CA 94305, USA; Perinatal Institute, Division of Pulmonary Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA; Center for Stem Cell and Organoid Medicine, CuSTOM, Division of Developmental Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.

Cell Stem Cell
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PubMed
Summary

Hypoplastic left heart syndrome (HLHS) involves impaired endocardium, crucial for heart development. This study reveals endocardial defects contribute to HLHS, suggesting new regenerative strategies.

Keywords:
ETS1NOTCHde novo mutationendocardiumendothelial to mesenchymal transitionfibronectinhuman heart tissuehypoplastic left heart syndromeinduced pluripotent stem cellssingle-cell RNA-seq

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Area of Science:

  • Cardiovascular Biology
  • Developmental Biology
  • Genetics

Background:

  • Hypoplastic left heart syndrome (HLHS) is a severe congenital heart defect affecting the left heart.
  • Existing research highlights myocardial defects but inadequately explains endocardial-derived structure abnormalities.

Purpose of the Study:

  • To identify endocardial defects in HLHS development.
  • To elucidate the role of endocardium in HLHS etiology and inform regenerative strategies.

Main Methods:

  • Single-cell RNA profiling of hiPSC-derived endocardium.
  • Analysis of human fetal heart tissue from HLHS cases.

Main Results:

  • Identified a developmentally impaired endocardial population in HLHS.
  • Found intrinsic endocardial defects impacting endothelial-to-mesenchymal transition, NOTCH signaling, and ECM organization.
  • Demonstrated endocardial abnormalities disrupt fibronectin-integrin signaling, affecting cardiomyocyte proliferation and maturation.

Conclusions:

  • Endocardium plays a critical role in HLHS pathogenesis.
  • Endocardial dysfunction is a key contributor to HLHS.
  • Findings support considering endocardial function in developing regenerative therapies for HLHS.