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Related Concept Videos

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...
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...
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)...
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...
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...

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Related Experiment Video

Updated: May 23, 2026

A Model of Disturbed Flow-Induced Atherosclerosis in Mouse Carotid Artery by Partial Ligation and a Simple Method of RNA Isolation from Carotid Endothelium
11:00

A Model of Disturbed Flow-Induced Atherosclerosis in Mouse Carotid Artery by Partial Ligation and a Simple Method of RNA Isolation from Carotid Endothelium

Published on: June 23, 2010

Compromised LCAT function is associated with increased atherosclerosis.

G Kees Hovingh1, Barbara A Hutten, Adriaan G Holleboom

  • 1Department of Vascular Medicine, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands.

Circulation
|August 3, 2005
PubMed
Summary
This summary is machine-generated.

Individuals with LCAT gene defects have low HDL cholesterol and high triglycerides, increasing cardiovascular disease risk. Targeting LCAT may offer a new strategy for CVD prevention.

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Related Experiment Videos

Last Updated: May 23, 2026

A Model of Disturbed Flow-Induced Atherosclerosis in Mouse Carotid Artery by Partial Ligation and a Simple Method of RNA Isolation from Carotid Endothelium
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A Model of Disturbed Flow-Induced Atherosclerosis in Mouse Carotid Artery by Partial Ligation and a Simple Method of RNA Isolation from Carotid Endothelium

Published on: June 23, 2010

Quantitative Analysis and Characterization of Atherosclerotic Lesions in the Murine Aortic Sinus
06:43

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

Published on: December 8, 2013

Quantification of Atherosclerosis in Mice
06:59

Quantification of Atherosclerosis in Mice

Published on: June 12, 2019

Area of Science:

  • Biochemistry
  • Genetics
  • Cardiovascular Medicine

Background:

  • Low HDL cholesterol is a known risk factor for cardiovascular disease (CVD).
  • The role of severely reduced HDL cholesterol, due to lecithin:cholesterol acyltransferase (LCAT) gene mutations, in CVD risk remains unclear.
  • Understanding CVD risk in LCAT mutation carriers may reveal LCAT as a therapeutic target.

Purpose of the Study:

  • To investigate the association between LCAT gene mutations and cardiovascular risk factors.
  • To assess cardiovascular risk markers in individuals with LCAT gene defects.

Main Methods:

  • Assessed lipids, lipoproteins, C-reactive protein (CRP), and carotid artery intima-media thickness (IMT).
  • Compared 47 heterozygotes for LCAT gene mutations with 58 family controls.
  • Statistical analysis adjusted for age, gender, and alcohol use.

Main Results:

  • Heterozygotes showed a 36% decrease in HDL cholesterol, a 23% increase in triglycerides, and a 2.1-fold increase in CRP.
  • Carotid IMT was significantly increased in heterozygotes compared to controls (P<0.0015 after adjustment).

Conclusions:

  • LCAT gene defects are linked to low HDL cholesterol, elevated triglycerides, and increased CRP.
  • The observed increase in IMT suggests LCAT protects against atherosclerosis.
  • Targeting LCAT to increase HDL cholesterol may be a viable strategy for reducing CVD risk.