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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...
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The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
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Chronic Inflammation: Introduction

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...
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...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...

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Updated: May 8, 2026

Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages
06:52

Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages

Published on: May 21, 2018

Inflammasome and atherogenesis.

Xinjie Lu, Vijay Kakkar1

  • 1Thrombosis Research Institute, London, SW3 6LR. xlu@tri-london.ac.uk.

Current Pharmaceutical Design
|August 16, 2013
PubMed
Summary
This summary is machine-generated.

Inflammasomes activate inflammatory cytokines, driving atherosclerosis progression. Targeting these pathways may offer new therapeutic strategies for this complex arterial disease.

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Last Updated: May 8, 2026

Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages
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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:

  • Immunology
  • Cardiovascular Biology
  • Molecular Medicine

Background:

  • Atherosclerosis involves lipid and immune cell accumulation in arteries.
  • Inflammation and innate immunity are key in early lesion development.
  • The inflammasome complex activates key inflammatory cytokines.

Purpose of the Study:

  • To review the role of inflammasomes in atherosclerosis pathogenesis.
  • To highlight IL-1β and IL-18's function in disease progression.
  • To identify potential molecular targets for atherosclerosis therapy.

Main Methods:

  • Literature review of inflammasome activation in atherosclerosis.
  • Analysis of cytokine signaling pathways (IL-1β, IL-18).
  • Examination of inflammasome's link to adaptive immunity.

Main Results:

  • Inflammasome activation drives key inflammatory processes in atherosclerosis.
  • IL-1β and IL-18 are crucial mediators of atherosclerotic plaque development.
  • Inflammasome components bridge innate and adaptive immunity in disease.

Conclusions:

  • Inflammasome-mediated inflammation is central to atherosclerosis.
  • Targeting inflammasomes and their downstream cytokines presents therapeutic opportunities.
  • Further research into inflammasome pathways could yield novel treatments.