Department of Neurology, Second Hospital of Hebei Medical University, 215 Hepingxi Road, Shijiazhuang, 050000, Hebei, China.
Mol Neurobiol. 2024 Dec;61(12):10736-10746. doi: 10.1007/s12035-024-04218-0. Epub 2024 May 23.
At present, it appears that the prognosis for subarachnoid haemorrhage (SAH), which has a high death and disability rate, cannot be greatly improved by medication or other treatment. Recent research suggests that different types of cell death are implicated in early brain injury (EBI) after SAH, and this has been recognised as a major factor impacting the prognosis of SAH. Ferroptosis, which is a recently identified imbalance of iron metabolism and programmed cell death triggered by phospholipid peroxidation, has been shown to be involved in EBI after SAH and is thought to have a significant impact on EBI. The decomposition of cleaved haemoglobin during SAH involves the release of enormous amounts of free iron, resulting in iron metabolism disorders. Potential therapeutic targets for the signalling pathways of iron metabolism disorders and ferroptosis after SAH are constantly being discovered. To serve as a guide for research into other possible therapeutic targets, this paper will briefly describe the mechanisms of dysregulated iron metabolism and ferroptosis in the pathogenesis of SAH and highlight how they are involved in the development and promotion of EBI in SAH.
目前，蛛网膜下腔出血（SAH）的预后似乎无法通过药物或其他治疗方法得到显著改善，SAH 的死亡率和致残率都很高。最近的研究表明，细胞死亡的不同类型与 SAH 后的早期脑损伤（EBI）有关，这已被认为是影响 SAH 预后的主要因素。铁死亡是一种最近发现的铁代谢失衡和由磷脂过氧化引发的程序性细胞死亡，已被证明与 SAH 后的 EBI 有关，并且被认为对 EBI 有重大影响。SAH 期间血红蛋白的分解会释放大量游离铁，导致铁代谢紊乱。SAH 后铁代谢紊乱和铁死亡信号通路的潜在治疗靶点不断被发现。为了为研究其他可能的治疗靶点提供指导，本文将简要描述 SAH 发病机制中失调的铁代谢和铁死亡的机制，并强调它们如何参与 SAH 中 EBI 的发展和促进。
