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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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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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Telomere dynamics during aging in polygenic left ventricular hypertrophy.

Francine Z Marques1, Scott A Booth1, Priscilla R Prestes1

  • 1School of Applied and Biomedical Sciences, Faculty of Science and Technology, Federation University Australia, Victoria, Australia;

Physiological Genomics
|October 29, 2015
PubMed
Summary

Longer neonatal telomeres in hypertrophic heart rats may indicate fewer early cell divisions, predisposing them to heart failure. Shorter telomeres were observed during hypertrophy but not at heart failure progression.

Keywords:
TercTertcardiac hypertrophydevelopmentleft ventricular hypertrophymiRNAtelomerasetelomeres

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Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Genetics of Heart Disease

Background:

  • Short telomeres are linked to increased cardiovascular disease risk.
  • Telomere length and telomerase activity are critical for cardiomyocyte health and cardiac function.
  • Understanding telomere dynamics in heart failure development is crucial for therapeutic strategies.

Purpose of the Study:

  • To investigate cardiomyocyte telomere length and related molecular factors during the development of cardiac hypertrophy and heart failure in the hypertrophic heart rat (HHR) model.
  • To compare telomere dynamics in HHR with a normal heart rat (NHR) control strain at key developmental and pathophysiological stages.
  • To explore the role of telomerase activity, gene expression (Tert, Terc), and microRNA (miR-34a) in HHR cardiac aging and disease progression.

Main Methods:

  • Measurement of telomere length in cardiac tissue at specific ages (2 days, 13 weeks, 38 weeks) in HHR and NHR rats.
  • Assay of tissue telomerase activity and quantification of mRNA levels for telomerase reverse transcriptase (Tert) and telomerase RNA component (Terc).
  • Analysis of microRNA miR-34a expression and correlation of circulating leukocyte telomere length with cardiac telomere length.

Main Results:

  • HHR rats exhibited longer cardiac telomeres at 2 days and 38 weeks, but shorter telomeres at 13 weeks compared to NHR.
  • Neonatal HHR showed higher cardiac telomerase activity and Tert/miR-34a expression, while Tert/Terc were overexpressed at 38 weeks.
  • miR-34a was upregulated at 13 weeks but downregulated at 38 weeks in HHR; cardiac telomere length correlated with leukocyte telomere length only in HHR.

Conclusions:

  • Longer neonatal telomeres in HHR likely result from reduced early cardiomyocyte proliferation, contributing to a lower cell count and predisposition to hypertrophy and failure.
  • While shorter telomeres characterize cardiac hypertrophy at 13 weeks, this is not sustained during the progression to heart failure at 38 weeks.
  • Telomere dynamics, influenced by telomerase and miR-34a, play a complex role in the ontogeny of cardiac hypertrophy and heart failure in the HHR model.