Emerging role of PARP-1 and PARthanatos in ischemic stroke

Shuiqiao Liu, Weibo Luo, Yingfei Wang

Research output: Contribution to journalReview articlepeer-review

19 Scopus citations


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. (Figure presented.).

Original languageEnglish (US)
Pages (from-to)74-87
Number of pages14
JournalJournal of Neurochemistry
Issue number1
StatePublished - Jan 2022

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience


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