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Related Concept Videos

Atherosclerosis I: Introduction01:30

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...
Atherosclerosis II: Clinical Manifestations and Diagnostic Tests01:27

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)...
Inflammation01:38

Inflammation

Overview
Peripheral Artery Disease I: Introduction01:30

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...
Amyloid Fibrils03:03

Amyloid Fibrils

Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
Amyloid deposits were observed as early as 1639 in the liver and the spleen.   In 1854, Rudolph Virchow performed iodine staining, normally used to...
Amyloid Fibrils03:03

Amyloid Fibrils

Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
Amyloid deposits were observed as early as 1639 in the liver and the spleen.   In 1854, Rudolph Virchow performed iodine staining, normally used to...

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Related Experiment Video

Updated: May 31, 2026

Cell-free Biochemical Fluorometric Enzymatic Assay for High-throughput Measurement of Lipid Peroxidation in High Density Lipoprotein
07:29

Cell-free Biochemical Fluorometric Enzymatic Assay for High-throughput Measurement of Lipid Peroxidation in High Density Lipoprotein

Published on: October 12, 2017

Serum amyloid A in atherosclerosis.

Victoria L King1, Joel Thompson, Lisa R Tannock

  • 1Division of Cardiovascular Medicine, Lexington, Kentucky, USA. Lisa.Tannock@uky.edu

Current Opinion in Lipidology
|July 8, 2011
PubMed
Summary

Serum amyloid A (SAA) may causally contribute to atherosclerosis development. This review explores evidence for SAA's role in cardiovascular disease, distinct from reflecting underlying risk factors.

Area of Science:

  • Biochemistry
  • Cardiovascular Medicine
  • Immunology

Background:

  • Serum amyloid A (SAA) proteins are acute-phase reactants linked to cardiovascular disease.
  • The precise role of SAA in atherosclerosis pathogenesis remains incompletely understood.
  • SAA presence in atherosclerotic lesions and adipose tissue suggests potential local contributions.

Purpose of the Study:

  • To review experimental evidence investigating a causal link between SAA and atherosclerosis.
  • To differentiate SAA's potential direct role from its function as a marker of disease.

Main Methods:

  • Review of recent experimental studies on SAA and atherosclerosis.
  • Analysis of SAA localization within vascular and adipose tissues.
  • Examination of SAA's association with different lipoprotein particles (HDL, apoB).

Related Experiment Videos

Last Updated: May 31, 2026

Cell-free Biochemical Fluorometric Enzymatic Assay for High-throughput Measurement of Lipid Peroxidation in High Density Lipoprotein
07:29

Cell-free Biochemical Fluorometric Enzymatic Assay for High-throughput Measurement of Lipid Peroxidation in High Density Lipoprotein

Published on: October 12, 2017

Main Results:

  • SAA is found within atherosclerotic lesions and adipose tissue.
  • Localized SAA synthesis in vasculature or adipose tissue may influence disease development.
  • SAA's association with HDL and apoB-lipoproteins may alter its biological activity.

Conclusions:

  • Emerging evidence supports a causal role for SAA in atherosclerosis.
  • Further research is needed to elucidate SAA's specific mechanisms in atherogenesis.