Abstract
The deletion of the gene coding for poly(ADP-ribose) polymerase-1 (PARP1) or its pharmacological inhibition protects mice against cerebral ischemia and Parkinson’s disease. In sharp contrast, PARP1 inhibitors are in clinical use for the eradication of vulnerable cancer cells. It appears that excessive PARP1 activation is involved in a specific cell death pathway called parthanatos, while inhibition of PARP1 in cancer cells amplifies DNA damage to a lethal level. Hence, PARP1 plays a context-dependent role in cell fate decisions. In addition, it appears that PARP1 plays an ambiguous role in organismal aging.
Original language | English |
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Pages (from-to) | 1-6 |
Number of pages | 6 |
Journal | Cell Stress |
Volume | 7 |
Issue number | 1 |
DOIs | |
Publication status | Published - 1 Jan 2023 |
Keywords
- DNA damage
- PARP1 inhibition
- aging
- cancer
- cellular stress response
- neurological diseases
- parthanatos