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Necrosis01:16

Necrosis

Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become anucleated and die, but their...
Cellular Injury IV: Necrosis01:16

Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...
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...
Overview of Cell Death01:30

Overview of Cell Death

Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the 20th century...
Cellular Injury IlI: Cellular Death01:11

Cellular Injury IlI: Cellular Death

Cell death is the irreversible loss of cellular structure and function, representing the final stage of severe injury. It plays a key role in both normal physiology and disease.Types of Cell DeathThe two main types are necrosis and apoptosis, though others like necroptosis and pyroptosis also exist.Necrosis:Necrosis is an unregulated form of cell death caused by severe injury such as trauma, toxins, or ischemia. It is characterized by cell swelling, membrane loss, rupture, and leakage of...

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Updated: Jun 1, 2026

Single Nuclei Isolation from Coronary Endarterectomy Tissue of Coronary Artery Bypass Graft Patients
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Necrotic cell death in atherosclerosis.

Wim Martinet1, Dorien M Schrijvers, Guido R Y De Meyer

  • 1Division of Pharmacology, University of Antwerp, Universiteitsplein 1, 2610 Antwerp, Belgium. wim.martinet@ua.ac.be

Basic Research in Cardiology
|May 26, 2011
PubMed
Summary

Necrosis, a cell death form, is increasingly recognized as regulated, not accidental. In atherosclerosis, necrotic cells promote inflammation and plaque instability, highlighting potential therapeutic targets.

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Area of Science:

  • Cardiovascular Biology
  • Cell Death Mechanisms
  • Pathology

Background:

  • Necrosis, characterized by cell swelling and membrane rupture, was historically viewed as uncontrolled cell death.
  • Emerging evidence indicates that necrosis can be a regulated process.
  • Morphological studies reveal necrosis as the predominant cell death mode in advanced human atherosclerotic plaques.

Purpose of the Study:

  • To investigate the role of regulated necrosis in atherosclerosis.
  • To understand the stimuli triggering necrotic cell death within atherosclerotic plaques.
  • To explore the contribution of necrosis to plaque progression and instability.

Main Methods:

  • Transmission electron microscopy for morphological analysis of dying cells in atherosclerotic plaques.
  • Analysis of cellular stimuli within the plaque microenvironment, including oxidative stress, ATP depletion, and calcium levels.

Main Results:

  • The majority of dying cells in advanced atherosclerotic plaques exhibit necrotic morphology.
  • Plaque-associated stimuli such as oxidative stress and impaired apoptotic cell clearance contribute to necrotic cell death.
  • Necrotic cell death stimulates atherogenesis by inducing inflammation and expanding the necrotic core.
  • Necrosis exacerbates plaque instability through the release of tissue factor, proteases, and pro-angiogenic factors.

Conclusions:

  • Necrosis plays a significant, regulated role in the pathogenesis of atherosclerosis.
  • Necrotic cell death promotes inflammation, necrotic core expansion, and plaque instability.
  • Targeting necrotic pathways or their inflammatory consequences represents a potential therapeutic strategy for atherosclerosis.