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...

Amyloid Fibrils

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,...

Amyloid Fibrils

Amyloid Fibrils

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...

Inflammation

Inflammation

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...

You might also read

Related Articles

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

Sort by

Same author

Independent and joint effects of ambient temperature and relative humidity on fetal distress: effect modification by air pollutants.

International journal of biometeorology·2026

Same author

Pseudomonas aeruginosa 3-oxo-C12HSL-induced apoptosis involves bitter taste receptor T2R14 and the mitochondrial calcium uniporter.

Cell calcium·2026

Same author

Identification of scavenger receptor BI as a scavenger of free heme that is essential for protection against hemolysis.

bioRxiv : the preprint server for biology·2026

Same author

Water-soluble hexagonal BaAl<sub>2</sub>O<sub>4</sub> as sacrificial layer for freestanding crystalline membranes and flexible devices.

Nature materials·2026

Same author

Strain-Assembled Crystalline SrRuO<sub>3</sub> Microtube and Emergent Curvilinear Magnetism.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)·2026

Same author

Mechanisms of Mitochondrial Toxicity and Cytotoxicity Caused by Pseudomonas aeruginosa Pyocyanin in Human Nasal Epithelial Cells.

International forum of allergy & rhinology·2025

Search research articles

Related Experiment Video

Updated: Feb 18, 2026

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

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

Published on: October 12, 2017

Serum amyloid A3 is pro-atherogenic.

Joel C Thompson¹, Patricia G Wilson¹, Preetha Shridas²

¹Department of Veterans Affairs, Lexington, KY 40502, USA; Department of Internal Medicine, University of Kentucky, Lexington, KY, 40536, USA; Barnstable Brown Diabetes Center, University of Kentucky, Lexington, KY, 40536, USA; Saha Cardiovascular Research Center, University of Kentucky, Lexington, KY, 40536, USA.

Atherosclerosis

|November 28, 2017

Summary

Serum amyloid A3 (SAA3) significantly increases atherosclerosis in mice. This finding resolves a paradox and supports the role of SAA in cardiovascular disease development.

Keywords:

Atherosclerosis Inflammation Murine models

More Related Videos

Rapid Generation of Amyloid from Native Proteins In vitro

Rapid Generation of Amyloid from Native Proteins In vitro

Published on: December 5, 2013

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

Published on: September 26, 2018

Related Experiment Videos

Last Updated: Feb 18, 2026

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

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

Published on: October 12, 2017

Rapid Generation of Amyloid from Native Proteins In vitro

Rapid Generation of Amyloid from Native Proteins In vitro

Published on: December 5, 2013

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

Published on: September 26, 2018

Area of Science:

Cardiovascular biology
Immunology
Molecular medicine

Background:

Serum amyloid A (SAA) is linked to cardiovascular events.
Murine SAA isoforms SAA1.1 and SAA2.1 deficiency do not impact atherosclerosis.
SAA3 is an expressed acute phase isoform in mice, unlike in humans.

Purpose of the Study:

To investigate the role of SAA3 in atherosclerosis development in mice.
To determine if SAA3 exacerbates or ameliorates atherosclerosis.

Main Methods:

ApoE knockout mice were utilized as the atherosclerosis model.
Adeno-associated virus mediated SAA3 overexpression.
Anti-sense oligonucleotide approach was used for SAA3 suppression.

Main Results:

SAA3 overexpression resulted in a 4-fold increase in atherosclerosis lesion area.
SAA3 suppression significantly decreased atherosclerosis in SAA1.1/SAA2.1 deficient mice.
Statistical significance was observed for both overexpression (p=0.01) and suppression (p<0.0001) studies.

Conclusions:

SAA3 plays a pro-atherogenic role in mice.
These findings reconcile existing literature and support epidemiological data on SAA and atherosclerosis.