Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Pathophysiology of Heart Failure

Pathophysiology of Heart Failure

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...

Heart Failure II: Pathophysiology

Heart Failure II: Pathophysiology

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...

Heart Failure I: Introduction

Heart Failure I: Introduction

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...

Heart Failure V: Medical Management

Heart Failure V: Medical Management

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...

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

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...

Cardiomyopathy II: Dilated Cardiomyopathy

Cardiomyopathy II: Dilated Cardiomyopathy

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,...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Decoding cardiotoxicity through proteomics and metabolomics: cathepsin C and amino acids take centre stage.

European heart journal·2026

Same author

Molecular Imaging of Mechanisms of Impaired Cardiac Repair After Macrophage Depletion in Mice: A Longitudinal Multitracer Imaging Study.

Journal of nuclear medicine : official publication, Society of Nuclear Medicine·2026

Same author

Artificial Intelligence in Biomedical Scientific Publishing.

European heart journal·2026

Same author

Mutation-dependent responses to sleep and exercise in clonal haematopoiesis.

Nature·2026

Same author

Preclinical Evaluation of Berry Extracts as a Nutritional Intervention to Alleviate Myocardial Ischemia-Reperfusion Injury and Atherosclerosis Development.

Phytotherapy research : PTR·2026

Same author

Pathophysiology, prevention, and management of coronary microvascular obstruction.

European heart journal·2026

Search research articles

Related Experiment Video

Updated: Sep 8, 2025

Analyzing Ex Vivo Metabolic Flux in Splenic and Cardiac Macrophages and Bone Marrow Monocytes

Analyzing Ex Vivo Metabolic Flux in Splenic and Cardiac Macrophages and Bone Marrow Monocytes

Published on: March 28, 2025

Immunometabolism in heart failure.

Ioanna Andreadou¹, Alessandra Ghigo², Panagiota-Efstathia Nikolaou¹

¹Laboratory of Pharmacology, School of Pharmacy, National and Kapodistrian University of Athens, Athens, Greece.

Nature Reviews. Cardiology

|June 21, 2025

Summary

This summary is machine-generated.

Heart failure involves complex interactions between inflammation and metabolism (immunometabolism). Understanding these pathways is key to developing new therapies that promote healing and improve patient outcomes.

More Related Videos

Author Spotlight: New Insights into PBMC Mitochondrial Responses Using Fluorespirometry

Author Spotlight: New Insights into PBMC Mitochondrial Responses Using Fluorespirometry

Published on: May 24, 2024

Implantation of an Isoproterenol Mini-Pump to Induce Heart Failure in Mice

Implantation of an Isoproterenol Mini-Pump to Induce Heart Failure in Mice

Published on: October 3, 2019

Related Experiment Videos

Last Updated: Sep 8, 2025

Analyzing Ex Vivo Metabolic Flux in Splenic and Cardiac Macrophages and Bone Marrow Monocytes

Analyzing Ex Vivo Metabolic Flux in Splenic and Cardiac Macrophages and Bone Marrow Monocytes

Published on: March 28, 2025

Author Spotlight: New Insights into PBMC Mitochondrial Responses Using Fluorespirometry

Author Spotlight: New Insights into PBMC Mitochondrial Responses Using Fluorespirometry

Published on: May 24, 2024

Implantation of an Isoproterenol Mini-Pump to Induce Heart Failure in Mice

Implantation of an Isoproterenol Mini-Pump to Induce Heart Failure in Mice

Published on: October 3, 2019

Area of Science:

Cardiovascular Medicine
Immunology
Metabolic Science

Background:

Inflammation and metabolism (immunometabolism) are central to heart failure pathophysiology, regardless of origin (ischemia or metabolic disorders) or ejection fraction.
Immune cell infiltration and polarization in the myocardium are driven by metabolic shifts, influencing cardiac and systemic metabolism.
This immune-metabolic crosstalk contributes to adverse cardiac remodeling and chronic inflammation, perpetuating heart failure progression.

Purpose of the Study:

To provide a comprehensive overview of the cellular and molecular mechanisms governing immunometabolism in heart failure.
To discuss current and potential therapeutic strategies targeting immunometabolism in heart failure.
To explore non-invasive monitoring and treatment approaches for heart failure patients.

Main Methods:

Review of existing literature on immunometabolism in heart failure.
Analysis of cellular and molecular pathways involved in immune cell infiltration and metabolic shifts.
Discussion of pharmacological and immunomodulatory interventions.

Main Results:

Identified bidirectional metabolic crosstalk between immune cells and cardiac cells contributing to adverse remodeling.
Highlighted the role of metabolic shifts in immune cell polarization (pro-inflammatory vs. anti-inflammatory).
Emphasized the perpetuation of chronic inflammation through myelopoiesis driven by injury and metabolic dysregulation.

Conclusions:

Understanding immunometabolism is crucial for developing novel heart failure therapies.
Targeting metabolic pathways and immune responses offers potential for improved patient outcomes.
Further research is needed to overcome challenges in immunomodulatory approaches and develop effective monitoring strategies.