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Related Concept Videos

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

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...
Heart Failure V: Medical Management01:30

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 II: Pathophysiology01:29

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...
Pathophysiology of Heart Failure01:17

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 VI: Adjunct Therapies01:22

Heart Failure VI: Adjunct Therapies

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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Related Experiment Video

Updated: Jun 11, 2026

Herbal Munziq Ameliorates Myocardial Ischemia-Reperfusion Injury by Inhibiting Inflammation
09:53

Herbal Munziq Ameliorates Myocardial Ischemia-Reperfusion Injury by Inhibiting Inflammation

Published on: January 10, 2025

Targeting S100A8/A9 Ameliorates Heart Failure with Preserved Ejection Fraction by Modulating TLR4/NF-κB-Mediated

Yansong Li1,2, Qi Han1, Xianling Liu1,2

  • 1Department of Geriatrics, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.

Clinical and Experimental Pharmacology & Physiology
|June 9, 2026
PubMed
Summary

Inhibition of S100A8/A9 inflammatory mediator improved diastolic dysfunction in heart failure with preserved ejection fraction (HFpEF) mice. This suggests S100A8/A9 is a potential therapeutic target for HFpEF via the TLR4/NF-κB pathway.

Keywords:
HFpEFS100A8/A9TLR4/NF‐κBInflammation

Related Experiment Videos

Last Updated: Jun 11, 2026

Herbal Munziq Ameliorates Myocardial Ischemia-Reperfusion Injury by Inhibiting Inflammation
09:53

Herbal Munziq Ameliorates Myocardial Ischemia-Reperfusion Injury by Inhibiting Inflammation

Published on: January 10, 2025

Area of Science:

  • Cardiology
  • Immunology
  • Pharmacology

Background:

  • Heart failure with preserved ejection fraction (HFpEF) is a growing global health concern with limited treatment options.
  • S100A8/A9 is an inflammatory mediator implicated in cardiovascular diseases through the TLR4/NF-κB pathway.
  • Understanding S100A8/A9's role in HFpEF is crucial for developing new therapies.

Purpose of the Study:

  • To investigate the role of S100A8/A9 in the development of HFpEF.
  • To explore the potential therapeutic effects of inhibiting S100A8/A9 in a mouse model of HFpEF.
  • To elucidate the underlying mechanisms involving the TLR4/NF-κB pathway.

Main Methods:

  • An HFpEF mouse model was created using a high-fat diet and L-NAME.
  • Mice were treated with paquinimod, an S100A8/A9 inhibitor, for 8 weeks.
  • Cardiac function, hypertrophy, fibrosis, inflammation, oxidative stress, and the TLR4/NF-κB pathway were assessed.

Main Results:

  • Paquinimod treatment improved diastolic dysfunction in HFpEF mice.
  • Inhibition of S100A8/A9 reduced cardiomyocyte hypertrophy, cardiac fibrosis, inflammation, and oxidative stress.
  • Paquinimod suppressed the TLR4/NF-κB signaling pathway, and TLR4 inhibition partly reversed HFpEF phenotypes.

Conclusions:

  • Inhibiting S100A8/A9 ameliorates HFpEF pathology and improves diastolic function in mice.
  • The therapeutic effects are potentially mediated by the inhibition of the TLR4/NF-κB pathway.
  • S100A8/A9 represents a promising therapeutic target for treating HFpEF.