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Overview of Cell Death01:30

Overview of Cell Death

7.9K
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...
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The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

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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...
6.7K
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

6.9K
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...
6.9K
Autophagic Cell Death01:18

Autophagic Cell Death

3.6K
Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...
3.6K
Necrosis01:16

Necrosis

4.9K
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...
4.9K
Apoptosis01:30

Apoptosis

12.0K
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...
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Related Experiment Video

Updated: Sep 20, 2025

Evaluation of Caspase Activation to Assess Innate Immune Cell Death
10:23

Evaluation of Caspase Activation to Assess Innate Immune Cell Death

Published on: January 20, 2023

3.4K

Reovirus Activated Cell Death Pathways.

Carly DeAntoneo1,2, Pranav Danthi3, Siddharth Balachandran1

  • 1Blood Cell Development and Function Program, Fox Chase Cancer Center, Philadelphia, PA 19111, USA.

Cells
|June 10, 2022
PubMed
Summary
This summary is machine-generated.

Mammalian orthoreoviruses (ReoV) induce programmed cell death (PCD) in tumor cells. New research shows ReoV activates necroptosis, a key inflammatory PCD, enhancing its oncolytic potential against cancer.

Keywords:
MLKLRIPK3ZBP1apoptosisnecroptosisoncolysisreovirus

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Area of Science:

  • Virology
  • Immunology
  • Oncology

Background:

  • Mammalian orthoreoviruses (ReoV) are non-enveloped viruses with double-stranded RNA genomes.
  • ReoV is generally non-pathogenic in humans but can cause mild gastroenteritis and contribute to inflammatory conditions like Celiac disease.
  • ReoV strain Type 3 Dearing (T3D) is being investigated as an oncolytic agent due to its ability to infect and kill cancer cells.

Purpose of the Study:

  • To review the ReoV replication cycle and its mechanisms for inducing programmed cell death (PCD).
  • To explore the role of non-apoptotic PCD pathways, particularly necroptosis, in ReoV pathogenesis and oncolysis.
  • To discuss the implications of ReoV-induced necroptosis for anti-tumor immunity.

Main Methods:

  • Review of existing literature on ReoV replication, PCD induction, and oncolytic mechanisms.
  • Analysis of studies investigating ReoV's interaction with various PCD pathways, including apoptosis, autophagy, pyroptosis, and necroptosis.
  • Examination of the molecular players in necroptosis, such as RIPK3 and MLKL, in the context of ReoV infection.

Main Results:

  • ReoV infection triggers multiple PCD pathways, challenging the previous assumption that apoptosis is dominant.
  • ReoV activates necroptosis, a caspase-independent inflammatory cell death pathway.
  • ReoV-induced necroptosis promotes tumor cell lysis and may enhance anti-tumor immune responses by inflaming the tumor microenvironment.

Conclusions:

  • ReoV utilizes diverse PCD mechanisms, including necroptosis, to achieve oncolysis.
  • Necroptosis plays a significant role in the therapeutic potential of ReoV as an oncolytic virus.
  • Understanding ReoV-induced necroptosis is crucial for optimizing its use in cancer therapy and harnessing its immunomodulatory effects.