Molecular mechanisms of neuronal death in brain injury after subarachnoid hemorrhage

Junhui Chen; Mingchang Li; Zhuanghua Liu; Yuhai Wang; Kun Xiong

doi:10.3389/fncel.2022.1025708

Molecular mechanisms of neuronal death in brain injury after subarachnoid hemorrhage

Front Cell Neurosci. 2022 Dec 13:16:1025708. doi: 10.3389/fncel.2022.1025708. eCollection 2022.

Authors

Junhui Chen^{1

2

3}, Mingchang Li², Zhuanghua Liu³, Yuhai Wang³, Kun Xiong¹

Affiliations

¹ Department of Human Anatomy and Neurobiology, School of Basic Medical Science, Central South University, Changsha, Hunan, China.
² Department of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, China.
³ Department of Neurosurgery, 904th Hospital of Joint Logistic Support Force of PLA, Wuxi Clinical College of Anhui Medical University, Wuxi, China.

Abstract

Subarachnoid haemorrhage (SAH) is a common cerebrovascular disease with high disability and mortality rates worldwide. The pathophysiological mechanisms involved in an aneurysm rupture in SAH are complex and can be divided into early brain injury and delayed brain injury. The initial mechanical insult results in brain tissue and vascular disruption with hemorrhages and neuronal necrosis. Following this, the secondary injury results in diffused cerebral damage in the peri-core area. However, the molecular mechanisms of neuronal death following an aneurysmal SAH are complex and currently unclear. Furthermore, multiple cell death pathways are stimulated during the pathogenesis of brain damage. Notably, particular attention should be devoted to necrosis, apoptosis, autophagy, necroptosis, pyroptosis and ferroptosis. Thus, this review discussed the mechanism of neuronal death and its influence on brain injury after SAH.

Keywords: SAH; apoptosis; autophagy; cell death; ferroptosis; necrosis; pyroptosis.

Publication types

Review