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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...
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...
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...
Inflammation01:38

Inflammation

Overview
Hypertension II: Pathophysiology01:29

Hypertension II: Pathophysiology

Hypertension is a chronic condition in which the blood's force against artery walls is excessively high, posing risks such as heart disease. The condition's underlying mechanisms involve complex interactions among the cardiovascular, kidney, and autonomic nervous systems.Renin-Angiotensin-Aldosterone System (RAAS): This system significantly influences blood pressure regulation. When blood pressure decreases, the kidneys secrete renin. This enzyme transforms angiotensinogen, a plasma protein,...

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Related Experiment Video

Updated: Jul 19, 2026

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
05:51

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology

Published on: May 6, 2014

Histamine network in atherosclerosis.

Akihide Tanimoto1, Yasuyuki Sasaguri, Hiroshi Ohtsu

  • 1Department of Pathology and Cell Biology, University of Occupational and Environmental Health, School of Medicine, Yahatanishi-ku, Kitakyushu 807-8555, Japan.

Trends in Cardiovascular Medicine
|October 24, 2006
PubMed
Summary

Histamine production in atherosclerosis is reduced in mice lacking histidine decarboxylase. Further research is needed to clarify histamine

Related Experiment Videos

Last Updated: Jul 19, 2026

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
05:51

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology

Published on: May 6, 2014

Area of Science:

  • Biochemistry
  • Immunology
  • Cardiovascular Research

Background:

  • Histamine, synthesized from l-histidine, is implicated in atherosclerotic lesions.
  • Its precise role and sources within these lesions remain incompletely understood.
  • Genetically engineered mouse models offer a valuable tool to investigate such complex biological processes.

Purpose of the Study:

  • To investigate the role of histamine in the development of atherosclerosis.
  • To identify the cellular sources of histamine within atherosclerotic lesions.
  • To explore the involvement of histamine receptors in the atherosclerotic process.

Main Methods:

  • Utilized histidine decarboxylase-gene knockout mice and wild-type control mice.
  • Compared the extent of atherosclerotic regions between the two groups.
  • Discussed potential cellular sources including macrophages, endothelial cells, and mast cells.

Main Results:

  • Histidine decarboxylase-gene knockout mice exhibited ameliorated atherosclerotic regions compared to wild-type controls.
  • This suggests a pro-atherogenic role for histamine produced via histidine decarboxylase.

Conclusions:

  • Histamine decarboxylase plays a role in promoting atherosclerosis.
  • Macrophages, endothelial cells, and mast cells are potential sources of histamine in atherosclerotic lesions.
  • Further investigation into the roles of all four histamine receptors (H1-H4) in atherosclerosis is warranted, particularly the recently cloned H3 and H4 receptors.