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Emerging role of PARP‐1 and PARthanatos in ischemic stroke
Author(s) -
Liu Shuiqiao,
Luo Weibo,
Wang Yingfei
Publication year - 2022
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/jnc.15464
Subject(s) - poly adp ribose polymerase , programmed cell death , biology , stroke (engine) , ischemia , neuroscience , disease , microbiology and biotechnology , bioinformatics , apoptosis , medicine , gene , polymerase , pathology , genetics , engineering , mechanical engineering
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.