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Inflammation

Inflammation

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...

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...

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)...

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Updated: May 10, 2026

Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions

Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions

Published on: October 17, 2017

Foam cells in atherosclerosis.

Xiao-Hua Yu¹, Yu-Chang Fu, Da-Wei Zhang

¹Life Science Research Center, University of South China, Hengyang, Hunan 421001, China.

Clinica Chimica Acta; International Journal of Clinical Chemistry

|June 21, 2013

Summary

This summary is machine-generated.

Macrophage foam cell formation in atherosclerosis involves an imbalance in cholesterol processes. Understanding cholesterol uptake, esterification, and efflux is key to developing new treatments for this chronic arterial disease.

Keywords:

ABCA1 ABCG1 ACAT1 AGE ATP-binding cassette transporter A1 ATP-binding cassette transporter G1 Atherosclerosis CD36 CE ERK1/2 FC Foam cells HDL LDLR LXR MAPK PI3K PKB PKC PPAR response elements PPAR-γ PPREs RCT RXR SR-A SR-BI TGF-β acyl coenzyme A:cholesterol acyltransferase-1 advanced glycation end products apoA-I apoE apolipoprotein A-I apolipoprotein E cholesterol ester extracellular signal-regulated kinases 1 and 2 free cholesterol high-density lipoprotein liver X receptor low-density lipoprotein receptor mitogen-activated protein kinase nCEH neutral cholesteryl ester hydrolase ox-LDL oxidized low-density lipoprotein peroxisome proliferator-activated receptor-γ phosphatidylinositol 3-kinase protein kinase B protein kinase C retinoid X receptor reverse cholesterol transport scavenger receptor BI scavenger receptor class A transforming growth factor-β

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Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions

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Quantitative Analysis and Characterization of Atherosclerotic Lesions in the Murine Aortic Sinus

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Published on: December 7, 2013

Area of Science:

Cardiovascular Biology
Cellular Metabolism
Atherosclerosis Research

Background:

Atherosclerosis is a chronic disease driven by cholesterol buildup in arteries.
Macrophage foam cells are central to atherosclerosis development, arising from cholesterol imbalance.
Key processes include cholesterol uptake, esterification, and efflux within macrophages.

Purpose of the Study:

To review the mechanisms of cholesterol uptake, esterification, and release in macrophages.
To highlight the roles of specific proteins in macrophage cholesterol homeostasis.
To provide a foundation for novel therapeutic strategies against atherosclerosis.

Main Methods:

This review synthesizes existing knowledge on macrophage cholesterol metabolism.
It examines the functions of key proteins involved in cholesterol transport and modification.
Literature review focusing on molecular mechanisms of foam cell formation.

Main Results:

CD36 and scavenger receptor class A (SR-A) mediate cholesterol uptake.
Acyl coenzyme A:cholesterol acyltransferase-1 (ACAT1) and neutral cholesteryl ester hydrolase (nCEH) regulate cholesterol esterification.
ATP-binding cassette transporters (ABCA1, ABCG1) and scavenger receptor BI (SR-BI) are critical for cholesterol efflux.

Conclusions:

Dysregulation of cholesterol influx, esterification, and efflux leads to macrophage foam cell formation.
Understanding these mechanisms is crucial for developing targeted therapies for atherosclerosis.
Further research into macrophage cholesterol pathways may yield novel treatment interventions.