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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,...
Caspases01:24

Caspases

Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside cells.
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...
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...
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.

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Related Experiment Video

Updated: Jul 11, 2026

Live-cell Imaging of Lysosomal Membrane Permeabilization During Necroptosis
05:30

Live-cell Imaging of Lysosomal Membrane Permeabilization During Necroptosis

Published on: November 14, 2025

Necrosis and the serpin under't.

Mary C Abraham1, Shai Shaham

  • 1Laboratory of Developmental Genetics, The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA.

Developmental Cell
|October 11, 2007
PubMed
Summary

A newly identified gene, previously thought to be a protease inhibitor, may prevent necrotic cell death. This finding challenges previous understandings of cell death pathways and protease functions.

Area of Science:

  • Molecular Biology
  • Cell Death Pathways
  • Protease Function

Background:

  • Caspase proteases are key mediators of apoptosis (programmed cell death).
  • Other proteases are known to be involved in necrotic cell death.
  • The precise molecular mechanisms regulating necrosis are less understood than apoptosis.

Purpose of the Study:

  • To investigate the role of a gene suspected to be a natural protease inhibitor.
  • To determine if this gene product influences necrotic cell death pathways.
  • To explore novel regulators of cell death beyond caspases.

Main Methods:

  • Analysis of gene expression and protein function.
  • Cellular assays to monitor cell death phenotypes.
  • Genetic manipulation to assess the impact of the gene on necrosis.

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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

Related Experiment Videos

Last Updated: Jul 11, 2026

Live-cell Imaging of Lysosomal Membrane Permeabilization During Necroptosis
05:30

Live-cell Imaging of Lysosomal Membrane Permeabilization During Necroptosis

Published on: November 14, 2025

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

Main Results:

  • Findings presented by Luke et al. (2007) in Cell indicate a novel function for the studied gene.
  • The gene product, initially characterized as a protease inhibitor, demonstrates a role in preventing necrosis.
  • This suggests a complex regulatory network controlling different modes of cell death.

Conclusions:

  • A gene previously identified as a protease inhibitor has a significant role in suppressing necrosis.
  • This discovery expands the known functions of protease inhibitors and implicates them in regulating cell death.
  • Further research is warranted to elucidate the precise molecular mechanisms by which this gene prevents necrosis.