[Mitochondrial mechanisms of apoptosis in response to DNA damage].
Integrity of genome is a prerequisite for cell viability. Therefore, targeted damage of DNA structure is considered the key approach to the induction of cell death. Among the plethora of death execution programs the mitochondrial events are of the utmost importance. However, the epigemetic activation of defense mechanisms in response to DNA damage limit cell death. This review analyses the outcome of the genotoxic stress (i.e., cell death versus survival) as a balance of pro- and anti-apoptotic signaling. Practically speaking, the combinations of DNA damaging agents with the inhibitors of anti-apoptosis would increase the efficacy of anticancer therapy.
Glazunova
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Shtil'
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D017209:Apoptosis / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D002453:Cell Cycle / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D004249:DNA Damage / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D004260:DNA Repair / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D004272:DNA, Mitochondrial / Q000378:metabolism; D044127:Epigenesis, Genetic / Q000502:physiology; D006801:Humans; D008928:Mitochondria / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
D004272:DNA, Mitochondrial; D019253:Proto-Oncogene Proteins c-bcl-2; D016159:Tumor Suppressor Protein p53