Rinald John H, Troy Carol M
Neurobiology and Behavior PhD Program, Columbia University, New York, NY, United States.
Department of Pathology and Cell Biology, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY, United States.
Front Cell Dev Biol. 2025 Apr 28;13:1570569. doi: 10.3389/fcell.2025.1570569. eCollection 2025.
Hemorrhagic stroke is a debilitating neurological disease, affecting millions worldwide. Characterized by bleeding in the brain, it is caused by a breakdown of the blood-brain barrier (BBB) and causes damage through the presence of iron in the brain, immune activation and increased intracranial pressure. The goal of this mini-review is to explore the signaling pathways that lead to cell death that are a part of disease progression in hemorrhagic stroke. This mini-review will highlight clinical observations and data, while also incorporating findings using preclinical disease models. There are important roles for apoptosis, necroptosis, necrosis, autophagy, ferroptosis, and pyroptosis in hemorrhagic stroke. Recent work has highlighted the interplay between these phenomena, providing key regulators as potential therapeutic targets, including reactive oxygen species, iron metabolism, and caspases. Therapeutic strategies that can delay or counteract the cytotoxic effects of hemorrhage can improve clinical outcomes in hemorrhagic stroke patients.
出血性中风是一种使人衰弱的神经疾病，影响着全球数百万人。其特征是脑部出血，由血脑屏障（BBB）的破坏引起，并通过脑内铁的存在、免疫激活和颅内压升高造成损害。本综述的目的是探讨导致细胞死亡的信号通路，这些通路是出血性中风疾病进展的一部分。本综述将突出临床观察和数据，同时纳入使用临床前疾病模型的研究结果。细胞凋亡、坏死性凋亡、坏死、自噬、铁死亡和细胞焦亡在出血性中风中都起着重要作用。最近的研究突出了这些现象之间的相互作用，提供了关键调节因子作为潜在的治疗靶点，包括活性氧、铁代谢和半胱天冬酶。能够延迟或抵消出血细胞毒性作用的治疗策略可以改善出血性中风患者的临床结局。
