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Related Concept Videos

Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

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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 Drugs: β-Blockers01:22

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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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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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Related Experiment Video

Updated: Aug 7, 2025

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β3AR-Dependent Brain-Derived Neurotrophic Factor (BDNF) Generation Limits Chronic Postischemic Heart Failure.

Alessandro Cannavo1,2, Seungho Jun1,3, Giuseppe Rengo1,4

  • 1Department of Translational Medical Science (A.C., G.R., F.M., D.L., A.E., N. Ferrara), University of Naples Federico II, Italy.

Circulation Research
|March 8, 2023
PubMed
Summary

Loss of brain-derived neurotrophic factor (BDNF) signaling contributes to heart disorders. TrkB agonists and beta-adrenergic receptor stimulation can restore BDNF levels, improving cardiac function after myocardial infarction.

Keywords:
brain-derived neurotrophic factorcardiac disordersheart failuremyocardial ischemiareceptors, adrenergic

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Area of Science:

  • Cardiovascular Biology
  • Neurobiology
  • Molecular Medicine

Background:

  • Brain-derived neurotrophic factor (BDNF)/TrkB signaling is crucial for neuronal and cardiac health.
  • Dysfunctional BDNF/TrkB signaling contributes to heart disorders, particularly after myocardial ischemia.
  • The role of BDNF in the postischemic heart and the therapeutic potential of TrkB agonists remain incompletely understood.

Purpose of the Study:

  • To investigate the role of BDNF in the postischemic myocardium.
  • To determine if TrkB agonists can counteract chronic left ventricle (LV) decompensation following myocardial infarction.
  • To explore the interplay between beta-adrenergic receptor stimulation and BDNF production in the heart.

Main Methods:

  • In vitro studies using cardiomyocytes, neuronal cells, and endothelial cells.
  • In vivo assessment of myocardial ischemia (MI) in wild type and genetically modified mice (β3AR knockout, myocyte-selective BDNF knockout).
  • Evaluation of isolated hearts subjected to global ischemia-reperfusion (I/R) injury.

Main Results:

  • Myocardial BDNF levels decreased significantly at 4 weeks post-MI, coinciding with LV dysfunction.
  • The TrkB agonist LM22A-4 improved cardiac function, reduced infarct size, and promoted neovascularization.
  • Beta-3 adrenergic receptor (β3AR) stimulation increased myocyte BDNF content, offering protection against I/R injury.
  • Beta-1 adrenergic receptor (β1AR) blockers, like metoprolol, improved chronic post-MI LV dysfunction by upregulating β3ARs and increasing myocardial BDNF.

Conclusions:

  • Loss of BDNF signaling contributes to chronic heart failure after ischemia.
  • TrkB agonists represent a potential therapeutic strategy to improve ischemic LV dysfunction by restoring myocardial BDNF.
  • Targeting cardiac β3ARs, either directly or indirectly via β-blockers, offers a novel BDNF-dependent approach to combat chronic postischemic heart failure.