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Related Concept Videos

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 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...
Chronic Inflammation: Introduction01:12

Chronic Inflammation: Introduction

Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
Myocarditis I: Introduction01:21

Myocarditis I: Introduction

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...
Rheumatic Heart Disease I: Introduction01:23

Rheumatic Heart Disease I: Introduction

Rheumatic heart disease or RHD is a chronic condition that results from rheumatic fever, causing permanent damage to the heart valves.Etiology and Risk FactorsIt primarily arises from rheumatic fever, an inflammatory disease that can develop after untreated or inadequately treated group A streptococcal (GAS) pharyngitis. Streptococcus spreads through direct contact with oral or respiratory secretions. While the bacteria are the causative agents, factors like malnutrition, overcrowding, poor...
Cellular Adaptation II: Hypertrophy01:26

Cellular Adaptation II: Hypertrophy

Hypertrophy is the increase in the size of individual cells, resulting in the enlargement of a tissue or organ. Unlike hyperplasia, which involves an increase in cell number, hypertrophy is characterized by an increase in cell volume. This process often occurs in response to higher functional demand or hormonal stimulation, leading to the production of more structural proteins and organelles, thereby enhancing the cells' work capacity.There are two primary types of hypertrophy: physiological...

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Related Experiment Video

Updated: Jun 28, 2026

Isolation of Macrophage Subsets and Stromal Cells from Human and Mouse Myocardial Specimens
07:25

Isolation of Macrophage Subsets and Stromal Cells from Human and Mouse Myocardial Specimens

Published on: December 17, 2019

Macrophage-Specific SPP1 Contributes to Pressure Overload-Induced Cardiac Dysfunction and Maladaptive Remodeling.

Weijian Ye1, Jia Sun2, Enzhao Shen3

  • 1Department of Pharmacy, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, China; School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, China.

JACC. Basic to Translational Science
|June 26, 2026
PubMed
Summary
This summary is machine-generated.

Researchers identified a specific macrophage subset that worsens heart damage after pressure overload. Blocking the HMGB1-NLRP3-SPP1 pathway with arglabin reduced inflammation and improved cardiac remodeling, offering a potential therapeutic target.

Keywords:
SPP1arglabincardiac remodelingmacrophagepressure overload

More Related Videos

Isolation and Culture of Resident Cardiac Macrophages from the Murine Sinoatrial and Atrioventricular Node
08:43

Isolation and Culture of Resident Cardiac Macrophages from the Murine Sinoatrial and Atrioventricular Node

Published on: May 7, 2021

Related Experiment Videos

Last Updated: Jun 28, 2026

Isolation of Macrophage Subsets and Stromal Cells from Human and Mouse Myocardial Specimens
07:25

Isolation of Macrophage Subsets and Stromal Cells from Human and Mouse Myocardial Specimens

Published on: December 17, 2019

Isolation and Culture of Resident Cardiac Macrophages from the Murine Sinoatrial and Atrioventricular Node
08:43

Isolation and Culture of Resident Cardiac Macrophages from the Murine Sinoatrial and Atrioventricular Node

Published on: May 7, 2021

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Molecular Medicine

Background:

  • Cardiac macrophages are key in myocardial remodeling but pathogenic subsets are unclear.
  • Understanding these subsets is crucial for treating heart disease.

Purpose of the Study:

  • Identify pathogenic macrophage subsets in pressure overload.
  • Elucidate the regulatory mechanisms driving cardiac pathogenesis.
  • Evaluate therapeutic targeting of identified pathways.

Main Methods:

  • Utilized transverse aortic constriction model in mice.
  • Investigated macrophage subpopulations and their secreted proteins.
  • Employed genetic deletion (Spp1) and pharmacological inhibition (arglabin).

Main Results:

  • Identified an early-emerging SPP1-expressing pathogenic macrophage subset.
  • Myeloid Spp1 deletion attenuated cardiac inflammation and dysfunction.
  • Discovered the HMGB1-NLRP3-NF-κB-SPP1 axis driving pathogenesis.
  • Arglabin inhibited this axis, reducing fibrosis and improving remodeling.

Conclusions:

  • A critical HMGB1-NLRP3-NF-κB-SPP1 axis in macrophages drives pressure overload-induced cardiac pathogenesis.
  • Targeting this axis, e.g., with arglabin, is a promising therapeutic strategy for pathological cardiac remodeling.