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

Atherosclerosis I: Introduction

Atherosclerosis I: Introduction

Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...

Autoimmune Disorders

Autoimmune Disorders

Autoimmune diseases are a group of disorders in which the body's immune system mistakenly attacks its own cells, tissues, and organs. This results from an overactive immune response against substances and tissues normally present in the body. Let's delve into the concept and mechanism of autoimmune diseases from an immune system point of view, explore different causes and examples of such diseases, and discuss potential solutions.
Concept and Mechanism of Autoimmune Diseases
The immune system...

Atherosclerosis II: Clinical Manifestations and Diagnostic Tests

Atherosclerosis II: Clinical Manifestations and Diagnostic Tests

Atherosclerosis is a progressive disorder that leads to the thickening and narrowing of arterial walls due to plaque buildup. This condition can cause various symptoms depending on the arteries affected:Coronary Artery Disease (CAD): This condition affects the coronary arteries and may lead to chest pain (angina), shortness of breath (dyspnea), heart attacks, and other heart disease symptoms.Cerebrovascular Disease: This affects blood flow to the brain, causing transient ischemic attacks (TIAs)...

Coronary Artery Disease II: Pathophysiology

Coronary Artery Disease II: Pathophysiology

Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...

Peripheral Artery Disease I: Introduction

Peripheral Artery Disease I: Introduction

Peripheral artery disease (PAD) predominantly results from atherosclerosis, which involves the accumulation of fatty deposits, or plaques, within the walls of arteries. This causes them to narrow and harden, significantly reducing blood flow. PAD predominantly affects the legs, particularly the arteries supplying the thighs and calves. In rare cases, it may involve other arteries, including those in the arms.Etiology of PAD:The principal cause of PAD is atherosclerosis, which results from fatty...

Atherosclerosis III: Management

Atherosclerosis III: Management

Management of atherosclerosis involves an integrated strategy encompassing pharmacological treatment, surgical interventions, lifestyle changes, and nutrition therapy to address the multifactorial nature of the disease.Pharmacological TherapyA cornerstone of atherosclerosis management is the use of pharmacological agents. Statins, such as atorvastatin, are pivotal in inhibiting HMG-CoA reductase, an enzyme that catalyzes an initial step in cholesterol synthesis in the liver. This reduction in...

You might also read

Related Articles

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

Sort by

Same author

RETRACTED: IDF23-0574 Role of urinary HO, 8-iso-PGF2α, and serum oxLDL/β2GP1 complex in the diabetic kidney disease.

Diabetes research and clinical practice·2025

Same author

CO<sub>2</sub> in indoor environments: From environmental and health risk to potential renewable carbon source.

The Science of the total environment·2022

Same author

Oviposition dynamics of Aedes aegypti in Central Argentina.

Medical and veterinary entomology·2021

Same author

The smart life.

The journal of primary prevention·2013

Same author

RUNX1, but not its familial platelet disorder mutants, synergistically activates PF4 gene expression in combination with ETS family proteins.

Journal of thrombosis and haemostasis : JTH·2013

Same author

Use of combination of rocuronium and sugammadex in heart transplant recipients.

Anaesthesia and intensive care·2012

Search research articles

Related Experiment Video

Updated: Jun 29, 2026

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology

Published on: May 6, 2014

Autoimmune-mediated atherothrombosis.

E Matsuura¹, L R Lopez

¹Department of Cell Chemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan. eijimatu@md.okayama-u.ac.jp

|October 2, 2008

Summary

This summary is machine-generated.

Oxidative stress in autoimmune diseases promotes the formation of oxidized low-density lipoprotein (oxLDL)/beta2GPI complexes. These complexes, along with their antibodies, accelerate atherosclerosis in conditions like lupus and antiphospholipid syndrome.

More Related Videos

Flow Cytometry Analysis of Immune Cells Within Murine Aortas

Flow Cytometry Analysis of Immune Cells Within Murine Aortas

Published on: July 1, 2011

Related Experiment Videos

Last Updated: Jun 29, 2026

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology

Published on: May 6, 2014

Flow Cytometry Analysis of Immune Cells Within Murine Aortas

Flow Cytometry Analysis of Immune Cells Within Murine Aortas

Published on: July 1, 2011

Area of Science:

Immunology
Cardiovascular Medicine
Rheumatology

Background:

Systemic autoimmune diseases often involve vascular inflammation and oxidative stress.
Oxidative stress leads to the modification of low-density lipoprotein (LDL) into oxidized LDL (oxLDL).
oxLDL can form complexes with beta2-glycoprotein I (beta2GPI), creating oxLDL/beta2GPI complexes.

Purpose of the Study:

To investigate the role of oxLDL/beta2GPI complexes in autoimmune vascular complications.
To explore the immunogenicity and atherogenic potential of oxLDL/beta2GPI complexes.
To understand the mechanism of macrophage uptake of these complexes.

Main Methods:

Detection of circulating oxLDL/beta2GPI complexes in patients with systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS).
Assessing the presence of antibodies against oxLDL/beta2GPI complexes.
Immunohistochemical staining of atherosclerotic lesions.
In vitro studies on macrophage uptake of oxLDL/beta2GPI complexes in the presence of antiphospholipid antibodies.

Main Results:

Circulating oxLDL/beta2GPI complexes and specific antibodies were found in SLE and APS patients.
These complexes appear to be formed in arterial walls and released into circulation.
Macrophage uptake of oxLDL/beta2GPI complexes increased with antiphospholipid antibodies, involving Fcgamma receptors.
This uptake promotes foam cell formation, explaining accelerated atherosclerosis.

Conclusions:

oxLDL/beta2GPI complexes and their antibodies are key players in autoimmune-mediated atherothrombosis.
These findings elucidate the accelerated atherosclerosis observed in SLE and APS.
The study highlights significant vascular injury and oxidative stress in these conditions.