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Related Concept Videos

Heart Failure VI: Adjunct Therapies01:22

Heart Failure VI: Adjunct Therapies

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Additional therapies for treating patients with heart failure (HF) may include procedural interventions, supplemental oxygen, the management of sleep disorders, and nutritional therapy.Procedural InterventionsImplantable Cardioverter-Defibrillator: For patients at risk of life-threatening arrhythmias due to severe left ventricular dysfunction, an Implantable Cardioverter-Defibrillator (ICD) can detect and terminate these arrhythmias, preventing sudden cardiac death and improving survival rates.
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Myocarditis III: Medical Management01:14

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Myocarditis: Comprehensive Medical ManagementMyocarditis, the heart muscle inflammation, requires a comprehensive medical management strategy that addresses the underlying cause, provides supportive care, manages symptoms, and reduces cardiac workload.Infections and Autoimmune CausesAdminister appropriate antimicrobial therapy when an infectious agent causes myocarditis. For instance, penicillin treats infections caused by Group A Streptococcus. In cases where autoimmune processes are...
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Myocarditis I: Introduction01:21

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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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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 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 III: Clinical Manifestations01:26

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Heart failure (HF) manifests primarily as dyspnea, fatigue, and fluid retention, resulting in peripheral and pulmonary edema. Symptoms may vary depending on which ventricle is more affected, left or right.Left-Sided Heart FailureAlso known as left ventricular failure, this condition results from the left ventricle's inability to fill or eject sufficient blood into the systemic circulation. It leads to pulmonary congestion, which occurs when the left ventricle fails to eject blood effectively...
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Updated: Jun 11, 2025

Benefits of Cardiac Resynchronization Therapy in an Asynchronous Heart Failure Model Induced by Left Bundle Branch Ablation and Rapid Pacing
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Interleukin 11 therapy causes acute left ventricular dysfunction.

Mark Sweeney1,2, Katie O'Fee1,2, Chelsie Villanueva-Hayes1,2

  • 1MRC-Laboratory of Medical Sciences, Hammersmith Hospital Campus, London W12 0NN, UK.

Cardiovascular Research
|October 9, 2024
PubMed
Summary
This summary is machine-generated.

Interleukin 11 (IL11) directly causes heart failure by activating IL11RA/JAK/STAT3 in cardiomyocytes. This finding overturns the previous belief that IL11 is cardioprotective and explains its severe cardiac side effects.

Keywords:
CardiotoxicityFibrosisHeart failureInflammationInterleukin 11JAK/STAT

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Area of Science:

  • Cardiology
  • Molecular Biology
  • Pharmacology

Background:

  • Interleukin 11 (IL11) was initially developed for thrombocytopenia treatment.
  • IL11 was later found redundant for hematopoiesis and linked to severe cardiac side effects.
  • Previous assumptions suggested IL11 was cardioprotective.

Purpose of the Study:

  • To identify direct cardiomyocyte toxicities of IL11.
  • To elucidate the molecular mechanisms underlying IL11-induced cardiac dysfunction.
  • To investigate the role of IL11RA/JAK/STAT3 signaling in IL11 cardiotoxicity.

Main Methods:

  • Recombinant mouse IL11 (rmIL11) injection in mice.
  • Molecular analyses including immunoblotting, qRT-PCR, bulk and single-cell RNA-seq, and ATAC-seq.
  • Cardiomyocyte-specific Il11ra1 knockout (CMKO) mouse models (vCMKO and m6CMKO).
  • Echocardiography, cardiomyocyte contractility assays, and JAK/STAT inhibition studies.

Main Results:

  • rmIL11 injection caused acute, dose-dependent impairment of left ventricular ejection fraction.
  • Increased myocardial STAT3 and JNK phosphorylation, pro-inflammatory pathways, and perturbed calcium handling.
  • Cardiomyocyte-specific knockout mice were protected from IL11-induced cardiac dysfunction.
  • JAK/STAT inhibition prevented rmIL11-induced cardiac toxicity.

Conclusions:

  • IL11 directly activates IL11RA/JAK/STAT3 signaling in cardiomyocytes, leading to acute heart failure.
  • These findings challenge the notion of IL11 as cardioprotective.
  • The study explains the severe cardiac side effects observed with IL11 therapy.