1. Emerging role of PARP‐1 and PARthanatos in ischemic stroke
- Author
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Yingfei Wang, Weibo Luo, and Shuiqiao Liu
- Subjects
Programmed cell death ,business.industry ,Poly ADP ribose polymerase ,Poly (ADP-Ribose) Polymerase-1 ,Ischemia ,Inflammation ,Brain damage ,medicine.disease_cause ,medicine.disease ,Biochemistry ,Article ,Energy homeostasis ,Cellular and Molecular Neuroscience ,Animals ,Humans ,Medicine ,medicine.symptom ,business ,Parthanatos ,Neuroscience ,Stroke ,Oxidative stress ,Ischemic Stroke - Abstract
Cell death is a key feature of neurological diseases, including stroke and neurodegenerative disorders. Studies in a variety of ischemic/hypoxic mouse models demonstrate that poly(ADP-ribose) polymerase 1 (PARP-1)-dependent cell death, also named PARthanatos, plays a pivotal role in ischemic neuronal cell death and disease progress. PARthanatos has its unique triggers, processors, and executors that convey a highly orchestrated and programmed signaling cascade. In addition to its role in gene transcription, DNA damage repair, and energy homeostasis through PARylation of its various targets, PARP-1 activation in neuron and glia attributes to brain damage following ischemia/reperfusion. Pharmacological inhibition or genetic deletion of PARP-1 reduces infarct volume, eliminates inflammation, and improves recovery of neurological functions in stroke. Here, we reviewed the role of PARP-1 and PARthanatos in stroke and their therapeutic potential.
- Published
- 2021