Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Heart Failure V: Medical Management01:30

Heart Failure V: Medical Management

204
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...
204
Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

693
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...
693
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

895
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...
895
Pathophysiology of Heart Failure01:17

Pathophysiology of Heart Failure

2.7K
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...
2.7K
Heart Failure Drugs: β-Blockers01:22

Heart Failure Drugs: β-Blockers

741
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,...
741
Heart Failure Drugs: Diuretics01:22

Heart Failure Drugs: Diuretics

775
Heart failure and kidney perfusion are interconnected in a complex way. Reduced renal perfusion and venous congestion are two significant factors that contribute to renal dysfunction in heart failure. The kidneys, primarily responsible for fluid balance in the body, are adversely affected due to compromised cardiac output and increased venous pressure. In response to reduced renal perfusion, the kidneys activate neurohumoral mechanisms to restore balance. However, these mechanisms can be...
775

You might also read

Related Articles

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

Sort by
Same author

The Rollercoaster of Research: A Day in the Life of Yuwei Jiang, University of Illinois Chicago, USA.

Comprehensive Physiology·2026
Same author

Drp1 regulates mitochondrial health and controls skeletal muscle mass through the Erk1/2-Nur77 pathway.

Science advances·2026
Same author

Age-dependent regulation of hematopoiesis by megakaryocytes.

Current opinion in hematology·2026
Same author

ERG-deficient endothelium identifies IL-8/CXCR2 axis as a therapeutic target for resolving neutrophilic lung vascular injury.

JCI insight·2026
Same author

Age-dependent progenitor switching shapes adult brown adipose tissue heterogeneity.

Research square·2026
Same author

ERα activates NAMPT/IL-33 signaling to enhance beige thermogenesis and metabolic fitness.

Science advances·2026

Related Experiment Video

Updated: Jan 10, 2026

Author Spotlight: Exploring the Relationship Between Lipotoxicity and HFpEF
03:42

Author Spotlight: Exploring the Relationship Between Lipotoxicity and HFpEF

Published on: March 29, 2024

2.0K

Targeting Adipose Tissue Function Protects Against Heart Failure with Preserved Ejection Fraction.

Jordan Jousma1, Zhenbo Han1, Jooman Park2

  • 1Department of Pharmacology & Regenerative Medicine, University of Illinois College of Medicine, Chicago, IL, 60612, USA.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|November 24, 2025
PubMed
Summary

Targeting thermogenic adipose tissue (AT) improves cardiac function in obesity-related heart failure with preserved ejection fraction (HFpEF). Activating or enhancing thermogenic AT offers a promising therapeutic strategy for cardiometabolic health.

Keywords:
HFpEFcardiometaboliclipidomicsobesitythermogenesis

More Related Videos

A Surgical Model of Heart Failure with Preserved Ejection Fraction in Tibetan Minipigs
07:09

A Surgical Model of Heart Failure with Preserved Ejection Fraction in Tibetan Minipigs

Published on: February 18, 2022

2.3K
Innovative Adipose Tissue Fractionation for Transforming Fat into Specialized Components
04:36

Innovative Adipose Tissue Fractionation for Transforming Fat into Specialized Components

Published on: July 11, 2025

1.1K

Related Experiment Videos

Last Updated: Jan 10, 2026

Author Spotlight: Exploring the Relationship Between Lipotoxicity and HFpEF
03:42

Author Spotlight: Exploring the Relationship Between Lipotoxicity and HFpEF

Published on: March 29, 2024

2.0K
A Surgical Model of Heart Failure with Preserved Ejection Fraction in Tibetan Minipigs
07:09

A Surgical Model of Heart Failure with Preserved Ejection Fraction in Tibetan Minipigs

Published on: February 18, 2022

2.3K
Innovative Adipose Tissue Fractionation for Transforming Fat into Specialized Components
04:36

Innovative Adipose Tissue Fractionation for Transforming Fat into Specialized Components

Published on: July 11, 2025

1.1K

Area of Science:

  • Cardiovascular Research
  • Metabolic Health
  • Adipose Tissue Biology

Background:

  • Obesity is a major risk factor for heart failure with preserved ejection fraction (HFpEF).
  • The role of thermogenic adipose tissue (AT) in obesity-related HFpEF remains unclear.
  • Understanding the adipose-heart axis is crucial for developing novel therapeutic strategies.

Purpose of the Study:

  • To investigate how targeting thermogenic adipose tissue (AT) influences cardiac function in a model of heart failure with preserved ejection fraction (HFpEF).
  • To evaluate the effects of pharmacological, surgical, and genetic interventions on thermogenic AT and cardiac outcomes.
  • To elucidate the underlying mechanisms connecting AT thermogenesis and cardiac health.

Main Methods:

  • Utilized a "two-hit" HFpEF mouse model.
  • Administered the β3-adrenergic receptor agonist CL-316,243 (CL) to activate thermogenic AT.
  • Employed genetic manipulations (Adipoq-Cre; Prdm16fl/fl and Ucp1-CreERT2; Cdkn2afl/fl) to suppress or enhance AT thermogenesis.
  • Performed lipidomic analysis (LC/MS-MS) to assess cardiac lipid profiles.
  • Conducted AT transplantation experiments.

Main Results:

  • Activation of thermogenic AT via CL improved cardiac function and reduced HFpEF-induced cardiac remodeling.
  • Enhanced energy expenditure was observed with thermogenic AT activation.
  • Transplantation of AT from CL-treated mice conferred cardioprotection.
  • Genetic suppression of thermogenesis abolished CL's beneficial effects.
  • Genetic enhancement of thermogenic AT improved cardiac structure and function.
  • AT thermogenesis significantly altered the cardiac lipidome.

Conclusions:

  • Thermogenic adipose tissue plays a critical role in mediating cardiac function in the context of obesity-related HFpEF.
  • Targeting the adipose-heart axis, specifically enhancing AT thermogenesis, represents a viable therapeutic approach for obesity-related HFpEF.
  • Alterations in the cardiac lipidome are mechanistically linked to the benefits of AT thermogenesis on heart health.