Ferroptosis in ischemic stroke: From a glia-neuron crosstalk perspective

Abstract

Stroke is renowned for its high rates of disability and mortality. Ischemic stroke (IS), the most prevalent type, imposes a heavy burden on patients. In recent years, ferroptosis has garnered significant interest in the field of neurological disease research and has been implicated in the pathophysiology of IS. This article provides a comprehensive review of the core mechanisms of ferroptosis. From the perspective of glia-neuron interactions, it explores iron metabolism, lipid peroxidation, and oxidative damage during IS, elucidating how these processes ultimately lead to ferroptosis and significant neuronal damage. Additionally, the emerging findings concerning the targets associated with ferroptosis in IS and related pharmacological therapies are described, thereby offering insights into innovative treatments for IS that focus on ferroptosis.