The Association between Ferroptosis and Glycolysis Following Subarachnoid Hemorrhage

Subarachnoid hemorrhage (SAH) is a brain disorder. Ferroptosis is a recently discovered type of regulated cell death. Glycolysis is a key energy-metabolism pathway in the brain, and disruptions in balance are thought to be at the origin of early brain injury. It is recent studies have shown that there are complex links between ferroptotic and glycolytic pathway and it is possible that the interaction can cause the resulting SAH-related brain injury; however, it is not clear what the precise molecular origin is.

This review summarizes the roles of ferroptosis and glycolysis in early brain injury (EBI) caused by subarachnoid hemorrhage (SAH) in the recent period, focusing on their mutual regulation and the impact on brain cell function or survival.

Recent results have shown how ferroptosis triggers neuronal apoptosis via iron overload and lipid peroxidation, while glycolytic metabolism also regulates cellular energy supply and the role of the antioxidant defense system. Ferroptosis, together with glycolysis, regulation of cellular energy metabolism, and expression of inflammatory factors, affects the survival and death of neurons and promotes the pathological process of EBI.

From the three dimensions of time, space, and cell type, we can formulate a comprehensive treatment strategy to jointly regulate ferroptosis and glycolysis, and dynamically monitor the early brain injury after subarachnoid hemorrhage.

The analysis provides a theoretical foundation and research directions for elucidating the pathological mechanisms of post-SAH brain injury and developing targeted therapeutic strategies.