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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...
Epigenetic Regulation01:37

Epigenetic Regulation

Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...
Epigenetic Regulation01:46

Epigenetic Regulation

Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
Epigenetic Regulation01:46

Epigenetic Regulation

Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
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...
Inflammation01:38

Inflammation

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Related Experiment Video

Updated: Jun 3, 2026

Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice
09:06

Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice

Published on: February 20, 2019

Atherosclerosis: an epigenetic balancing act that goes wrong.

Gertrud Lund1, Silvio Zaina

  • 1Department of Genetic Engineering, CINVESTAV, Unidad Irapuato, Km 9.6 Libramiento Norte Carretera Irapuato-León, 36500 Irapuato, Mexico. glund@ira.cinvestav.mx

Current Atherosclerosis Reports
|March 9, 2011
PubMed
Summary

Dietary lipids influence gene expression and inflammation by interacting with nuclear receptors. This review explores how dietary components can epigenetically promote atherosclerosis by altering gene activation and repression.

Related Experiment Videos

Last Updated: Jun 3, 2026

Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice
09:06

Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice

Published on: February 20, 2019

Area of Science:

  • Nutritional epigenetics
  • Molecular biology
  • Cardiovascular research

Background:

  • Dietary lipids modulate gene expression via nuclear receptors.
  • Nuclear receptors regulate lipid metabolism, inflammation, and vascular homeostasis.
  • Receptor activity depends on a balance between co-activator and co-repressor partners.

Purpose of the Study:

  • To review the role of dietary components in inducing atherosclerotic phenotypes.
  • To explore the concept of epigenetic modifications by diet.
  • To discuss how diet-induced epigenetic changes affect gene regulation.

Main Methods:

  • Literature review of studies on dietary lipids, nuclear receptors, and epigenetics.
  • Analysis of mechanisms linking diet, epigenetics, and atherosclerosis.
  • Discussion of gene activation and repression pathways.

Main Results:

  • Dietary components can impose epigenetic marks on DNA.
  • These epigenetic changes can alter the balance of gene activation and repression.
  • Aberrant epigenetic marks in promoter and intragenic regions may contribute to atherosclerosis.

Conclusions:

  • Dietary lipids are key modulators of inflammatory and metabolic gene expression.
  • Epigenetic mechanisms are involved in diet-induced atherosclerosis.
  • Dietary interventions targeting epigenetic modifications may offer therapeutic strategies.