Various modes of cell death induced by DNA damage

The consequences of DNA damage depend on the cell type and the severity of the damage. Mild DNA damage can be repaired with or without cell-cycle arrest. More severe and irreparable DNA injury leads to the appearance of cells that carry mutations or causes a shift towards induction of the senescence...

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Veröffentlicht in:Oncogene Jg. 32; H. 33; S. 3789 - 3797
Hauptverfasser: Surova, O, Zhivotovsky, B
Format: Journal Article
Sprache:Englisch
Veröffentlicht: London Nature Publishing Group UK 15.08.2013
Nature Publishing Group
Schlagworte:
631/337/1427
631/67/1059
631/80/82
Animals
Apoptosis
Autophagy
Cell Biology
Cell cycle
Cell death
Cell Death - physiology
Decision making
Deoxyribonucleic acid
DNA
DNA damage
DNA Damage - physiology
DNA repair
Gene expression
Genetic aspects
Human Genetics
Humans
Internal Medicine
Medicine
Medicine & Public Health
Necrosis
Oncology
review
Senescence
Signal transduction
Sweden
senescence
cell death
DNA damage
response
p53
ISSN:0950-9232, 1476-5594, 1476-5594
Online-Zugang:Volltext
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Beschreibung
Zusammenfassung:The consequences of DNA damage depend on the cell type and the severity of the damage. Mild DNA damage can be repaired with or without cell-cycle arrest. More severe and irreparable DNA injury leads to the appearance of cells that carry mutations or causes a shift towards induction of the senescence or cell death programs. Although for many years it was argued that DNA damage kills cells via apoptosis or necrosis, technical and methodological progress during the last few years has helped to reveal that this injury might also activate death by autophagy or mitotic catastrophe, which may then be followed by apoptosis or necrosis. The molecular basis underlying the decision-making process is currently the subject of intense investigation. Here, we review current knowledge about the response to DNA damage and subsequent signaling, with particular attention to cell death induction and the molecular switches between different cell death modalities following damage.
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ISSN:0950-9232
1476-5594
1476-5594
DOI:10.1038/onc.2012.556