Various modes of cell death induced by DNA damage
Abstract
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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Depending on cell type and intensity and nature of stress, cells may respond by inducing repair, cell death or senescence.
“Depending on the cell type and intensity and nature of the stress, cells may respond by inducing repair, cell death or senescence (Surova and Zhivotovsky, 2013; Galluzzi et al., 2018; Sapieha and Mallette, 2018).”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as Surova and Zhivotovsky, 2013
In absence of p53, mitotic defects can drive a necrotic variant of RCD independent of CASP2 signaling in some settings.
“In the absence of p53, however, mitotic defects appear to drive a necrotic variant of RCD independent of CASP2 signaling (at least in some settings) [990–992].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [992]
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- Authors
- Surova, O., & Zhivotovsky, B.
- Affiliations
- Karolinska Institutet (SE)
- Corresponding author
- Zhivotovsky, B
- Venue
- Oncogene
- Published
- 2012-12-03
- Volume
- 32
- Issue
- 33
- Pages
- 3789-3797
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- OpenAlex
- W2090408878
- Cited by
- 334
- References
- 72
- Citations by year
- 2026: 12 · 2025: 23 · 2024: 21 · 2023: 30 · 2022: 51 · 2021: 37 · 2020: 30 · 2019: 8 · 2018: 18 · 2017: 11 · 2016: 26 · 2015: 27 · 2014: 28 · 2013: 11
- FWCI
- 1.93
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Oncogene (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- DNA damage, cell death, apoptosis, necrosis, autophagy, mitotic catastrophe, cell cycle arrest, DNA repair, cellular senescence
- MeSH terms
- Animals, DNA Damage, Humans, Cell Death
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