Progress in Research on Regulated Cell Death in Cerebral Ischaemic Injury After Cardiac Arrest

Abstract

Ischaemic damage to the brain is the main cause of brain injury after cardiac arrest. The current treatment focuses on early reperfusion, but reperfusion tends to cause reperfusion injury, which is a significant problem. Cell death is an irreversible and normal end to cell life, playing key roles in maintaining the homeostasis and development of multicellular organisms. To date, cell death can be classified into two categories: accidental cell death (ACD) and regulated cell death (RCD). Cell death plays an indispensable role in cerebral ischaemia injury. An increasing number of scholars are exploring the mechanisms and sites of cell death during targeted inhibition of cerebral ischaemia to treat cerebral ischaemia injury. In addition to the established cell death pathways, namely, the apoptosis, pyroptosis and necroptosis pathways, ferroptosis and cuproptosis pathways have been discovered. This article reviews the cell death pathways involved in ischaemic brain injury, discusses the roles played by these death modalities, and suggests therapeutic directions for future targeting of cell death sites.