Related Experiment Video

Updated: Jun 27, 2026

Quantification of Atherosclerosis in Mice
06:59

Quantification of Atherosclerosis in Mice

Published on: June 12, 2019

Despite antiatherogenic metabolic characteristics, SCD1-deficient mice have increased inflammation and

Marcia L E MacDonald1, Miranda van Eck, Reeni B Hildebrand

  • 1Centre for Molecular Medicine and Therapeutics, Department of Medical Genetics, University of British Columbia, and Child & Family Research Institute, 980 West 28th Avenue, Vancouver, BC, Canada V5Z 4H4.

Arteriosclerosis, Thrombosis, and Vascular Biology
|December 20, 2008
PubMed
Abstract

Insights

Stearoyl-CoA desaturase-1 (SCD1) deficiency surprisingly worsens atherosclerosis in mice, despite improving metabolic health. This highlights inflammation

Area of Science:

  • Biochemistry
  • Immunology
  • Cardiovascular Science

Background:

  • Stearoyl-CoA desaturase-1 (SCD1) deficiency in mice improves metabolic health, reducing triglycerides, obesity, and insulin resistance.
  • This metabolic profile suggests reduced susceptibility to atherosclerosis.

Purpose of the Study:

  • To investigate the impact of SCD1 deficiency on the development of atherosclerosis.

Main Methods:

  • Utilized two models of SCD1-deficient mice, including low-density lipoprotein receptor (LDLR)-deficient mice on a Western diet.
  • Assessed atherosclerosis by measuring lesion area at the aortic root.
  • Analyzed inflammatory markers in skin, plasma, and macrophages.
  • Investigated the role of bone marrow-derived cells in SCD1-deficient atherosclerosis.

Main Results:

  • SCD1 deficiency significantly increased atherosclerosis in hyperlipidemic LDLR-deficient mice.
  • Increased lesion area was observed in both male and female mice.
  • Elevated inflammatory markers, including intercellular adhesion molecule (ICAM)-1 and interleukin-6, were found in plasma and skin.
  • High-density lipoprotein (HDL) particles showed inflammatory changes, with altered apolipoprotein and paraoxonase-1 levels.
  • SCD1 deficiency limited to bone marrow-derived cells did not alter lesion size.

Conclusions:

  • Chronic inflammation plays a critical role in promoting atherosclerosis, irrespective of favorable metabolic conditions.
  • SCD1 deficiency exacerbates atherosclerosis despite an antiatherogenic metabolic profile.

More Related Videos

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice07:36

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

Published on: September 26, 2018

Related Concept Videos

Inflammation01:38

Inflammation

Overview
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...
Coronary Artery Disease I: Introduction01:30

Coronary Artery Disease I: Introduction

Coronary Artery Disease (CAD): An Overview with Scientific InsightsCoronary Artery Disease (CAD), often referred to as C-A-D, is a prevalent blood vessel disorder classified under the broader category of atherosclerosis. Atherosclerosis is a pathological process characterized by the hardening and narrowing of arteries due to the accumulation of atherosclerotic plaques. These plaques are composed of cholesterol, fatty substances, inflammatory cells, calcium, and fibrin, reducing blood flow to...
Atherosclerosis III: Management01:26

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...
Coronary Artery Disease II: Pathophysiology01:26

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...
Inflammatory Bowel Disease III: Crohn's Disease01:25

Inflammatory Bowel Disease III: Crohn's Disease

Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...