Death through a tragedy: mitotic catastrophe

Vakifahmetoglu, H; Olsson, M; Zhivotovsky, B

doi:10.1038/cdd.2008.47

Cited by 700Cell death mechanisms and regulationMicrotubule and mitosis dynamicsCancer-related Molecular Pathways

Death through a tragedy: mitotic catastrophe

Vakifahmetoglu, H, Olsson, M, Zhivotovsky, B·2008·Cell Death & Differentiation

DOI 10.1038/cdd.2008.47

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Abstract

Mitotic catastrophe (MC) has long been considered as a mode of cell death that results from premature or inappropriate entry of cells into mitosis and can be caused by chemical or physical stresses. Whereas it initially was depicted as the main form of cell death induced by ionizing radiation, it is today known to be triggered also by treatment with agents influencing the stability of microtubule, various anticancer drugs and mitotic failure caused by defective cell cycle checkpoints. Although various descriptions explaining MC exist, there is still no general accepted definition of this phenomenon. Here, we present evidences indicating that death-associated MC is not a separate mode of cell death, rather a process ('prestage') preceding cell death, which can occur through necrosis or apoptosis. The final outcome of MC depends on the molecular profile of the cell.

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The caspase-dependent mechanisms responsible for phospholipid scrambling have been elusive.
“To date, the caspase-dependent mechanisms responsible for phospholipid scrambling have been elusive.”
From Immunogenic and tolerogenic cell death (2009) · cites this paper as [114]
Dying cells release soluble 'find me' signals that form a gradient attracting phagocytes.
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From Immunogenic and tolerogenic cell death (2009) · cites this paper as [114]
Three classes of event accompany cell death to promote engulfment.
“Three classes of event accompany cell death to promote engulfment89,114.”
From Immunogenic and tolerogenic cell death (2009) · cites this paper as [114]
Many cells express a 'don't eat me' signal that must be negated for phagocytosis to occur.
“Many cells express a “don’t eat me” signal, which must be negated for phagocytosis to occur.”
From Immunogenic and tolerogenic cell death (2009) · cites this paper as [114]
A number of bridging molecules have been identified that recognize phosphatidylserine and other eat-me signals.
“Instead, a number of bridging molecules have been identified that perform the recognition of this and other eat-me signals.”
From Immunogenic and tolerogenic cell death (2009) · cites this paper as [114]

Loss of ATP or permeabilization of the plasma membrane causes phosphatidylserine and other asymmetrically oriented phospholipids to diffuse to both leaflets.
“Loss of ATP or permeabilization of the plasma membrane results in diffusion of PS and other asymmetrically oriented phospholipids to both leaflets.”
From Immunogenic and tolerogenic cell death (2009) · cites this paper as [114]
During apoptosis or in response to signals such as calcium flux, rapid scrambling of membrane phospholipids occurs, causing loss of phospholipid asymmetry including appearance of phosphatidylserine on the outer leaflet.
“During apoptosis, or in response to other signals such as calcium flux, a more rapid “scrambling” of membrane phospholipids occurs, resulting in loss of phospholipids asymmetry including appearance of PS on the outer leaflet.”
From Immunogenic and tolerogenic cell death (2009) · cites this paper as [114]
As cells die they expose eat-me signals including oxidized lipids, changes in carbohydrate composition, and phosphatidylserine.
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From Immunogenic and tolerogenic cell death (2009) · cites this paper as [114]
Calreticulin is also expressed on dying cells.
“Calreticulin is also expressed on dying cells (see text).”
From Immunogenic and tolerogenic cell death (2009) · cites this paper as [114]
Receptors on phagocytes for these bridging molecules are the αvβ3 and αvβ5 integrins, the MER tyrosine kinase family, the scavenger receptors CD36 and SRA, and the C1q receptors CD91 and calreticulin.
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From Immunogenic and tolerogenic cell death (2009) · cites this paper as [114]
Other bridging molecules may include thrombospondin, C1q, and β2-GPI.
“Other bridging molecules may include thrombospondin, C1q, and β2-GPI.”
From Immunogenic and tolerogenic cell death (2009) · cites this paper as [114]

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Authors: Vakifahmetoglu, H., Olsson, M., & Zhivotovsky, B.
Affiliations: Karolinska Institutet (SE)
Corresponding author: Zhivotovsky, B
ORCID: Olsson, M
Zhivotovsky, B
Venue: Cell Death & Differentiation
Publisher: Springer Science and Business Media LLC
Published: 2008-04-11
Volume: 15
Issue: 7
Pages: 1153-1162
ISSN: 1350-9047 (ISSN-L)
1476-5403
DOI: 10.1038/cdd.2008.47
OpenAlex: W1997367417
Cited by: 700
References: 138
Citations by year: 2026: 20 · 2025: 38 · 2024: 31 · 2023: 42 · 2022: 40 · 2021: 41 · 2020: 37 · 2019: 26 · 2018: 40 · 2017: 41 · 2016: 49 · 2015: 35 · 2014: 42 · 2013: 60 · 2012: 51
FWCI: 2.76
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
www.springer.com/tdm (vor)
Locations: Cell Death and Differentiation (publishedVersion)
PubMed (publishedVersion)
Funders: Vetenskapsrådet
Barncancerfonden
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Microtubule and mitosis dynamics
Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Keywords: mitotic catastrophe, cell death, premature mitosis, ionizing radiation, microtubule stability, anticancer agents, cell cycle checkpoints, necrosis, apoptosis
MeSH terms: Animals, Cell Biology, DNA Damage, Humans, Microtubule Proteins, Mitosis, Necrosis, Terminology as Topic, Giant Cells, Cell Death, Apoptosis, Cell Cycle Proteins, History, 20th Century, History, 21st Century

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Death through a tragedy: mitotic catastrophe

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