Autophagy and Apoptosis Following Subarachnoid Hemorrhage

蛛网膜下腔出血(subarachnoid hemorrhage, SAH)通常由颅内动脉瘤破裂引起，是一种高死亡率和致残率的神经危重症。SAH后会触发一系列的病理级联反应，其中，细胞自噬和细胞凋亡作为两个重要的生物学过程，参与SAH后神经损伤的发生与发展。细胞自噬是细胞内部受损或衰老的细胞器及蛋白质成分降解的过程，对维持细胞稳态和生存具有重要作用，在SAH后可发挥一定的神经保护作用。细胞凋亡则是一种程序性细胞死亡方式，在SAH后脑损伤的多个病理生理过程中扮演着重要角色。细胞自噬可以减轻细胞凋亡的诱导，而细胞凋亡的激活又会抑制细胞自噬；但在特殊情况下，过度自噬则会加重细胞凋亡的发生。开发有效的靶点进而精准调控细胞自噬并抑制细胞凋亡，可为SAH患者提供更为有效的治疗手段。本文结合SAH的疾病背景，对细胞自噬与细胞凋亡以及两者之间关系的研究做一综述。Subarachnoid hemorrhage (SAH), typically caused by ruptured intracranial aneurysms, represents a critical neurological condition with high mortality and disability rates. SAH triggers a cascade of pathological reactions, in which autophagy and apoptosis emerge as two pivotal biological processes contributing to the initiation and progression of neuronal injury following SAH. Autophagy is a process by which damaged or aged organelles and protein components within cells are degraded. It plays a crucial role in maintaining cellular homeostasis and survival, and exerts certain neuroprotective effects after SAH. In contrast, apoptosis, a programmed cell death modality, critically participates in multiple pathophysiological pathways of SAH-induced brain injury. Autophagy demonstrates the capacity to mitigate apoptosis induction, while conversely, apoptotic activation may suppress autophagic processes; however, under specific pathological contexts, excessive autophagy paradoxically exacerbates apoptotic pathways. The development of effective therapeutic targets to precisely modulate autophagy while suppressing apoptosis holds significant potential for advancing treatment strategies for SAH patients. This review integrates the disease context of SAH to summarize current research on cellular autophagy, apoptosis, and their interrelationship.