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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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The heart's primary function is to pump blood throughout the body, maintaining a balance between blood sent out (cardiac output) and blood returning (venous return). If this balance is disrupted, it can result in congestive heart failure (CHF), a severe condition where the heart becomes an inefficient pump, leading to inadequate blood circulation.
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Glucose Homeostasis: Regulation of Blood Glucose01:02

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Carbohydrates consumed through foods are converted into glucose, a crucial energy source for the body. In the prandial state, high blood glucose levels stimulate the secretion of insulin from the pancreas. Insulin inhibits hepatic glucose production and stimulates glucose uptake and metabolism by muscle and adipose tissue. The excess glucose is converted into glycogen and stored in the liver and muscles.
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Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

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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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Pathophysiology of Heart Failure01:17

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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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Heart Failure Drugs: Inotropic Agents01:26

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Positive inotropic agents are commonly used as the first line of treatment for heart failure. One such agent is digoxin, derived from the genus Digitalis, which has been known for centuries but effectively utilized since 1785. However, these cardiac glycosides can have potentially toxic effects due to their mechanism of action, which involves inhibiting Na+/K+-ATPase and increasing contractility. Digoxin is absorbed orally and distributed in various tissues, including the CNS. It has a long...
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Related Experiment Video

Updated: Mar 6, 2026

Magnetic Adjustment of Afterload in Engineered Heart Tissues
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Transient elevation in cellular glucose uptake exacerbates pressure overload-induced cardiac hypertrophy and

Sayan Bakshi1,2, Samuel F Chang1,3, Luke A Potter1

  • 1Department of Pathology, Division of Molecular and Cellular Pathology, University of Alabama at Birmingham, Birmingham, AL, USA.

Epigenetics
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PubMed
Summary

Prior high blood sugar, known as glycemic memory, worsens heart problems after a second stress. Epigenetic changes like DNA methylation may drive these lasting cardiovascular effects, offering potential therapeutic targets.

Keywords:
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Glucose Uptake Measurement and Response to Insulin Stimulation in In Vitro Cultured Human Primary Myotubes
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Area of Science:

  • Cardiovascular Science
  • Metabolic Disease Research
  • Epigenetics

Background:

  • Prior hyperglycemia can cause long-term cardiovascular damage, termed 'glycemic memory.'
  • Epigenetic modifications, particularly DNA methylation, are hypothesized to mediate this phenomenon.
  • Understanding glycemic memory is crucial for preventing heart disease progression.

Purpose of the Study:

  • To investigate if prior high glucose exposure exacerbates cardiovascular effects under pressure overload.
  • To identify gene expression and DNA methylation signatures associated with glycemic memory in cardiomyocytes.
  • To explore potential therapeutic targets for heart failure susceptibility linked to hyperglycemia.

Main Methods:

  • Utilized inducible, cardiomyocyte-specific glucose transporter 4 (GLUT4) overexpressing mice.
  • Induced high glucose delivery, followed by a return to basal levels, then subjected mice to transverse aortic constriction (TAC) or sham surgery.
  • Assessed cardiac function, remodeling, gene expression (RNA-sequencing), and DNA methylation (bisulfite sequencing).

Main Results:

  • TAC exacerbated cardiac hypertrophy and dysfunction in high-glucose-exposed mice.
  • Persistent molecular changes, including altered gene expression and DNA methylation, were observed even after glucose levels normalized.
  • Enriched pathways indicated links between gene expression, DNA methylation, and adverse cardiac events, supporting the glycemic memory concept.

Conclusions:

  • Glycemic memory exacerbates cardiac structural and functional decline, mimicking heart failure under secondary stress.
  • Identified transcriptome and DNA methylome changes that may serve as molecular signatures of glycemic memory.
  • These findings suggest potential therapeutic targets for heart failure resulting from prior hyperglycemia.