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Related Concept Videos

Cholecystitis01:20

Cholecystitis

Cholecystitis is inflammation of the gallbladder, most commonly caused by obstruction of the cystic duct. This blockage prevents bile from draining, leading to gallbladder distension, inflammation, and potentially serious complications. This condition may present acutely or chronically and can happen with or without gallstones.EtiologyAbout 95% of cholecystitis cases are calculous, caused by gallstones blocking the cystic duct, leading to bile accumulation and inflammation of the gallbladder...
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Chronic Inflammation: Introduction01:12

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Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
Cholesterol: Significance and Regulation01:29

Cholesterol: Significance and Regulation

Although not a source of energy, cholesterol plays a significant role as a foundational structure for bile salts, steroid hormones, and vitamin D, as well as being a crucial component of plasma membranes. Approximately 15% of blood cholesterol is derived from our diet, with the remainder synthesized from acetyl CoA by the liver and intestines. Cholesterol is eliminated from the body through its conversion into bile salts, which are eventually discarded in the feces.
Considering cholesterol and...
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Chronic Pancreatitis I: Introduction01:25

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Differential Effects of Lipid-lowering Drugs in Modulating Morphology of Cholesterol Particles
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Differential Effects of Lipid-lowering Drugs in Modulating Morphology of Cholesterol Particles

Published on: November 10, 2017

Cholesterol crystals and inflammation.

Alena Grebe1, Eicke Latz

  • 1Institute of Innate Immunity, University Hospitals Bonn, Bonn, Germany. alena.grebe@uni-bonn.de

Current Rheumatology Reports
|February 16, 2013
PubMed
Summary
This summary is machine-generated.

Cholesterol crystals drive chronic vascular inflammation and atherosclerosis progression by activating immune responses and physically disrupting plaques. Understanding these mechanisms is key to developing cardiovascular disease treatments.

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Related Experiment Videos

Last Updated: May 14, 2026

Differential Effects of Lipid-lowering Drugs in Modulating Morphology of Cholesterol Particles
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Published on: November 10, 2017

Methods to Study Lipid Alterations in Neutrophils and the Subsequent Formation of Neutrophil Extracellular Traps
10:58

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Enrichment of Mammalian Tissues and Xenopus Oocytes with Cholesterol
10:12

Enrichment of Mammalian Tissues and Xenopus Oocytes with Cholesterol

Published on: March 25, 2020

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Lipid Metabolism

Background:

  • Chronic vascular inflammation is central to cardiovascular disease pathogenesis.
  • The precise triggers for vascular inflammation remain incompletely understood.
  • Excessive cholesterol accumulation initiates and advances atherosclerosis.

Purpose of the Study:

  • To review the role of cholesterol deposition and crystallization in cardiovascular disease.
  • To elucidate the mechanisms by which cholesterol crystals induce inflammatory responses.
  • To discuss the impact of cholesterol crystals on atherosclerotic plaque stability.

Main Methods:

  • Literature review of studies on cholesterol metabolism and inflammation in atherosclerosis.
  • Analysis of the molecular pathways involved in cholesterol crystal-mediated inflammasome activation.
  • Examination of evidence linking crystalline cholesterol to plaque rupture.

Main Results:

  • Cholesterol accumulation leads to macrophage foam cell formation.
  • Crystalline cholesterol activates the NLRP3 inflammasome, promoting interleukin-1 secretion.
  • Cholesterol crystals are implicated in the physical disruption and rupture of atherosclerotic plaques.

Conclusions:

  • Cholesterol crystallization is a significant driver of inflammatory responses in cardiovascular disease.
  • Activation of the NLRP3 inflammasome by cholesterol crystals contributes to disease progression.
  • Targeting cholesterol crystal-mediated inflammation may offer novel therapeutic strategies for atherosclerosis.