Molecular mechanisms of interaction between ferroptosis and cuproptosis in ischemic stroke. Pharmacological perspectives on preventing brain dysfunction

Ischemic stroke is one of the most severe and common neurological disorders, posing a significant threat to the health and life expectancy of affected individuals. Resulting from impaired blood flow, ischemic stroke leads to hypoxia and cerebral tissue ischemia, triggering a cascade of pathophysiological changes that markedly exacerbate neuronal damage and may ultimately result in cell death. New recent studies increasingly focus on newly discovered mechanisms of cell death, such as ferroptosis and cuproptosis. There is growing evidence supporting the independent roles of ferroptosis and cuproptosis in ischemic stroke. The aim of this review is to elucidate the potential mechanisms of cross-regulation between ferroptosis and cuproptosis and to investigate their regulatory roles in ischemic stroke. This review thoroughly examines intracellular interactions between ferroptosis and cuproptosis in ischemic stroke, emphasizing key aspects such as the fundamental roles of iron and copper, metabolic disturbances in ischemic stroke, cross-influences, and signaling pathways. Summarizing recent publications not only deepens our understanding of the pathogenesis of ischemic stroke but also suggests novel perspectives and directions for future pharmacological interventions in the treatment of ischemic stroke.