Generic placeholder image

Current Neuropharmacology


ISSN (Print): 1570-159X
ISSN (Online): 1875-6190

Review Article

P2X7 Receptor-Associated Programmed Cell Death in the Pathophysiology of Hemorrhagic Stroke

Author(s): Hengli Zhao, Yujie Chen* and Hua Feng

Volume 16, Issue 9, 2018

Page: [1282 - 1295] Pages: 14

DOI: 10.2174/1570159X16666180516094500

Price: $65


Hemorrhagic stroke is a life-threatening disease characterized by a sudden rupture of cerebral blood vessels, and cell death is widely believed to occur after exposure to blood metabolites or subsequently damaged cells. Recently, programmed cell death, such as apoptosis, autophagy, necroptosis, pyroptosis, and ferroptosis, has been demonstrated to play crucial roles in the pathophysiology of stroke. However, the detailed mechanisms of these novel kinds of cell death are still unclear. The P2X7 receptor, previously known for its cytotoxic activity, is an ATP-gated, nonselective cation channel that belongs to the family of ionotropic P2X receptors. Evolving evidence indicates that the P2X7 receptor plays a pivotal role in central nervous system pathology; genetic deletion and pharmacological blockade of the P2X7 receptor provide neuroprotection in various neurological disorders, including intracerebral hemorrhage and subarachnoid hemorrhage. The P2X7 receptor may regulate programmed cell death via (I) exocytosis of secretory lysosomes, (II) exocytosis of autophagosomes or autophagolysosomes during formation of the initial autophagic isolation membrane or omegasome, and (III) direct release of cytosolic IL-1β secondary to regulated cell death by pyroptosis or necroptosis. In this review, we present an overview of P2X7 receptor- associated programmed cell death for further understanding of hemorrhagic stroke pathophysiology, as well as potential therapeutic targets for its treatment.

Keywords: P2X7 receptor, apoptosis, autophagy, necroptosis, pyroptosis, intracerebral hemorrhage, subarachnoid hemorrhage.

Graphical Abstract

Rights & Permissions Print Export Cite as
© 2023 Bentham Science Publishers | Privacy Policy