Chen Junhui, Li Mingchang, Liu Zhuanghua, Wang Yuhai, Xiong Kun
Department of Human Anatomy and Neurobiology, School of Basic Medical Science, Central South University, Changsha, Hunan, China.
Department of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, China.
Front Cell Neurosci. 2022 Dec 13;16:1025708. doi: 10.3389/fncel.2022.1025708. eCollection 2022.
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.
蛛网膜下腔出血(SAH)是一种常见的脑血管疾病,在全球范围内具有较高的致残率和死亡率。SAH 中动脉瘤破裂所涉及的病理生理机制复杂,可分为早期脑损伤和延迟性脑损伤。最初的机械性损伤导致脑组织和血管破坏,伴有出血和神经元坏死。在此之后,继发性损伤导致核心周围区域的弥漫性脑损伤。然而,动脉瘤性 SAH 后神经元死亡的分子机制复杂,目前尚不清楚。此外,在脑损伤的发病机制中,多种细胞死亡途径被激活。值得注意的是,应特别关注坏死、凋亡、自噬、坏死性凋亡、细胞焦亡和铁死亡。因此,本综述讨论了 SAH 后神经元死亡的机制及其对脑损伤的影响。