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Related Concept Videos

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,...
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...
Inflammation01:38

Inflammation

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Chronic Inflammation: Introduction01:12

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...
Secondary Spinal Cord Injury llI: Pathophysiology01:25

Secondary Spinal Cord Injury llI: Pathophysiology

Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...
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Inflammatory Response

An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
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Related Experiment Video

Updated: May 27, 2026

Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis
08:55

Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis

Published on: August 7, 2018

Many stimuli pull the necrotic trigger, an overview.

N Vanlangenakker1, T Vanden Berghe, P Vandenabeele

  • 1Department for Molecular Biomedical Research, VIB, Zwijnaarde-Ghent, Belgium.

Cell Death and Differentiation
|November 15, 2011
PubMed
Summary
This summary is machine-generated.

Regulated necrosis, particularly necroptosis mediated by RIPK1/RIPK3 kinases, is a critical cellular defense. This review explores necroptosis inducers and its role in disease, highlighting RIPK1/RIPK3 as therapeutic targets.

Related Experiment Videos

Last Updated: May 27, 2026

Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis
08:55

Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis

Published on: August 7, 2018

Area of Science:

  • Cell Biology
  • Immunology
  • Molecular Medicine

Background:

  • Receptor-interacting protein kinase 1 (RIPK1) is crucial in caspase-independent cell death.
  • Regulated necrosis, especially RIPK1/RIPK3 kinase-mediated necroptosis, is a key cellular defense and implicated in disease.
  • Necroptosis acts as a backup to apoptosis and plays roles in viral defense and ischemia-reperfusion injury.

Purpose of the Study:

  • To review and discuss inducers of regulated necrosis.
  • To highlight the role of RIPK1 and RIPK3 in necroptosis.
  • To explore the therapeutic potential of targeting necroptosis.

Main Methods:

  • Literature review of regulated necrosis research.
  • Discussion of RIPK1 and RIPK3 roles in cell death pathways.
  • Analysis of RIPK3's role in controlling necroptosis during development.

Main Results:

  • RIPK1 is essential for caspase-independent cell death.
  • RIPK3 ablation rescues lethality in mice lacking apoptosis components, indicating its role in negative control of necroptosis.
  • Various inducers, including cytokines and cellular stress, trigger regulated necrosis.

Conclusions:

  • RIPK1 and RIPK3 are central to necroptosis, a significant regulated cell death pathway.
  • Necroptosis is involved in viral infections, inflammatory diseases, and ischemia-reperfusion damage.
  • RIPK1 and RIPK3 are promising therapeutic targets for treating various diseases.