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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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Myocarditis I: Introduction01:21

Myocarditis I: Introduction

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Myocarditis is inflammation of the myocardium, which is the muscular layer of the heart.EtiologyMyocarditis has a diverse etiology, including a wide range of infectious and non-infectious causes:Infectious CausesViral: Common viruses include Coxsackie A and B, adenovirus, parvovirus B19, enteroviruses, and influenza A.Bacterial: Examples include infections caused by Streptococcus, Staphylococcus, and Mycoplasma species.Rickettsial: Infections like Rocky Mountain spotted fever can result in...
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Pathophysiology of Heart Failure01:17

Pathophysiology of Heart Failure

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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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Cardiomyopathy II: Dilated Cardiomyopathy01:30

Cardiomyopathy II: Dilated Cardiomyopathy

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Dilated cardiomyopathy, or DCM, is a progressive myocardial disorder characterized by ventricular chamber dilation and contractile dysfunction.EtiologyVarious factors can cause DCM, including hypertension and heavy alcohol intake, which contribute to the weakening and enlargement of the heart muscle. Viral infections, such as Coxsackievirus B, adenoviruses, and influenza, can lead to DCM by causing inflammation and damage to heart tissue. Certain chemotherapeutic agents, including daunorubicin,...
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Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

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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 I: Introduction01:27

Heart Failure I: Introduction

179
Heart failure refers to a clinical syndrome caused by structural or functional cardiac disorders that prevent the heart from pumping an adequate amount of blood to meet the body's metabolic needs. This condition often arises from myocardial infarction or ischemia, leading to decreased cardiac output, reduced tissue perfusion, impaired gas exchange, fluid volume imbalance, and decreased functional ability.Heart failure can result from disruptions in the mechanisms that regulate cardiac output...
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Related Experiment Video

Updated: Nov 2, 2025

Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages
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AIM2-driven inflammasome activation in heart failure.

Zsófia Onódi1,2, Mihály Ruppert3, Dániel Kucsera1,2

  • 1Department of Pharmacology and Pharmacotherapy, Semmelweis University, Budapest, Hungary.

Cardiovascular Research
|June 12, 2021
PubMed
Summary

Inflammasome activation, specifically AIM2 and NLRC4, contributes to chronic heart failure (HF). The drug probenecid reduced inflammasome activation and alleviated HF in translational models, suggesting its potential for HF treatment.

Keywords:
CanakinumabCardiomyopathyDrug repurposingHeart failureInflammationProbenecid

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Area of Science:

  • Cardiovascular biology
  • Immunology
  • Inflammation research

Background:

  • Interleukin-1β (IL-1β) is a key factor in cardiovascular diseases like chronic heart failure (HF).
  • Inflammasomes, the source of IL-1β, are emerging therapeutic targets for cardiovascular diseases, as indicated by the CANTOS trial.

Purpose of the Study:

  • To investigate inflammasome activation patterns in failing hearts.
  • To identify specific inflammasome subtypes contributing to IL-1β production in HF.

Main Methods:

  • Assessed expression of four inflammasome sensors (AIM2, NLRC4, NLRP1, NLRP3) in human HF samples.
  • Utilized translational animal models of HF (rat and pig) to study inflammasome activation.
  • Investigated the effect of probenecid on AIM2 inflammasome activation in vitro and in vivo.

Main Results:

  • Absent in melanoma 2 (AIM2) and NLRC4 inflammasome expression increased in human HF.
  • AIM2 activation patterns in animal models mirrored those in human HF.
  • Probenecid reduced AIM2 activation in vitro and improved outcomes in a rat HF model.

Conclusions:

  • AIM2 and NLRC4 inflammasome activation are implicated in chronic inflammation in heart failure.
  • Probenecid demonstrates potential for alleviating chronic HF by reducing inflammasome activation.
  • Repurposing probenecid for heart failure indications is suggested by this translational study.