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β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation,...
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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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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: Inhibitors of Renin-Angiotensin System01:26

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The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
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Heart Failure V: Medical Management01:30

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Medical Management of Acute Decompensated Heart Failure (ADHF)The primary goals of therapy for patients hospitalized with acute decompensated heart failure (ADHF) include:Relieving symptomsOptimizing volume statusSupporting oxygenation and ventilationMaintaining cardiac output (CO) and end-organ perfusionIdentifying and addressing the cause of ADHFPreventing complicationsProviding patient education on factors precipitating HF exacerbationPlanning for dischargeOngoing monitoring and assessment...
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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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Heart Failure and MEF2 Transcriptome Dynamics in Response to β-Blockers.

S W Tobin1,2,3, S Hashemi1,2,3, K Dadson1

  • 1Department of Biology, York University, Toronto, ON, M3J 1P3, Canada.

Scientific Reports
|July 2, 2017
PubMed
Summary
This summary is machine-generated.

Myocyte Enhancer Factor 2 (MEF2) activity in heart failure (HF) was investigated. Beta-blocker treatment improved cardiac function and altered MEF2-regulated gene networks, revealing potential therapeutic targets for HF.

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Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Genomics

Background:

  • Myocyte Enhancer Factor 2 (MEF2) plays a key role in cardiac remodeling during heart failure (HF).
  • Beta-adrenergic signaling, a primary HF treatment, targets MEF2.
  • Understanding MEF2-mediated gene networks in HF is crucial for therapeutic development.

Purpose of the Study:

  • To identify global gene transcription networks regulated by MEF2 in heart failure.
  • To investigate the impact of beta-blocker treatment on these networks.
  • To uncover novel MEF2 target genes with potential diagnostic or therapeutic value in HF.

Main Methods:

  • Experimental heart failure induced by transverse aortic constriction (TAC) in mice.
  • Treatment with Atenolol (a beta-blocker) or solvent control.
  • Transcriptome analysis using RNA-sequencing on left ventricular samples and MEF2A-depleted cardiomyocytes.

Main Results:

  • Atenolol treatment improved cardiac function in TAC mice and repressed MEF2 activity.
  • TAC induced 65 differentially expressed genes (DEGs) related to inflammation, cell migration, and apoptosis.
  • Atenolol reversed the expression of 28 of these TAC-mediated DEGs.
  • Rarres2 was identified as a novel MEF2 target gene upregulated in HF and responsive to isoproterenol.

Conclusions:

  • MEF2 activity and its downstream gene networks are significantly altered in heart failure.
  • Beta-blocker therapy modulates these networks, offering therapeutic benefits.
  • Identified genes, including Rarres2, represent potential targets for heart failure diagnosis and treatment.