Autophagy and genomic integrity

DNA lesions, constantly produced by endogenous and exogenous sources, activate the DNA damage response (DDR), which involves detection, signaling and repair of the damage. Autophagy, a lysosome-dependent degradation pathway that is activated by stressful situations such as starvation and oxidative s...

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Bibliographic Details
Published in:Cell death and differentiation 2013-11, Vol.20 (11), p.1444-1454
Main Authors: Vessoni, A T, Filippi-Chiela, E C, Menck, C FM, Lenz, G
Format: Article
Language:English
Subjects:
631/208/211
631/337/1427
631/337/1427/2566
631/80/82/39
Animals
Apoptosis
Ataxia
Autophagy
Autophagy - genetics
Biochemistry
Biomedical and Life Sciences
Breast cancer
Carcinogenesis - genetics
Carcinogenesis - metabolism
Cell Biology
Cell Cycle Analysis
Cell death
DNA Damage
DNA Repair
DNA, Mitochondrial - genetics
DNA, Mitochondrial - metabolism
Genes
Genomic Instability
Homeostasis
Humans
Kinases
Life Sciences
Mitochondria
Mitochondrial DNA
Oxidative stress
Proteins
Review
Stem Cells
Tumorigenesis
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Summary:DNA lesions, constantly produced by endogenous and exogenous sources, activate the DNA damage response (DDR), which involves detection, signaling and repair of the damage. Autophagy, a lysosome-dependent degradation pathway that is activated by stressful situations such as starvation and oxidative stress, regulates cell fate after DNA damage and also has a pivotal role in the maintenance of nuclear and mitochondrial genomic integrity. Here, we review important evidence regarding the role played by autophagy in preventing genomic instability and tumorigenesis, as well as in micronuclei degradation. Several pathways governing autophagy activation after DNA injury and the influence of autophagy upon the processing of genomic lesions are also discussed herein. In this line, the mechanisms by which several proteins participate in both DDR and autophagy, and the importance of this crosstalk in cancer and neurodegeneration will be presented in an integrated fashion. At last, we present a hypothetical model of the role played by autophagy in dictating cell fate after genotoxic stress.
ISSN:1350-9047
1476-5403
DOI:10.1038/cdd.2013.103