Gong Yuhua, Yang Fumei, Liu Ying, Gong Yuping
School of Smart Health, Chongqing Polytechnic University of Electronic Technology, Chongqing, China.
Ultrasound Department of the Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Front Neurol. 2025 May 1;16:1508718. doi: 10.3389/fneur.2025.1508718. eCollection 2025.
Intracerebral hemorrhage (ICH) is an important neurological disease caused by the rupture of blood vessels in the brain parenchyma, with a high mortality and disability rate. At present, many studies have focused on the injury mechanisms and intervention strategies after ICH. However, there is no effective clinical treatment that can significantly improve the prognosis of ICH patients. Ferroptosis, a regulated form of cell death, has been identified as a significant contributor to brain tissues damage and neurological dysfunction following ICH. The hallmark of ferroptosis is iron-dependent lipid peroxidation, which is closely related to the pathological process of iron overload and oxidative stress after ICH. Exploring the interaction between ferroptosis and pathological injury mechanisms post-ICH will contribute to our understanding the key pathways involved in the ferroptosis-related injury mechanisms and facilitating the discovery of appropriate intervention strategies. On this basis, we present a comprehensive overview of ferroptosis-related brain injury mechanisms (e.g., iron overload, oxidative stress, inflammatory response and mass effect) in the pathogenesis and development of ICH. Following ICH, the degradation of hematoma and iron metabolism provide the fundamental material basis for ferroptosis, and oxidative stress primarily participates in the lipid peroxidation process of ferroptosis via related molecular pathways (such as the GPX4). By synthesizing current evidence, this article aims to provide a theoretical foundation for future research on therapeutic strategies targeting ferroptosis and related pathways in ICH.
脑出血（ICH）是一种由脑实质血管破裂引起的重要神经系统疾病，死亡率和致残率很高。目前，许多研究都集中在脑出血后的损伤机制和干预策略上。然而，尚无有效的临床治疗方法能够显著改善脑出血患者的预后。铁死亡是一种受调控的细胞死亡形式，已被确定为脑出血后脑组织损伤和神经功能障碍的重要原因。铁死亡的标志是铁依赖性脂质过氧化，这与脑出血后铁过载和氧化应激的病理过程密切相关。探索脑出血后铁死亡与病理损伤机制之间的相互作用，将有助于我们了解铁死亡相关损伤机制中涉及的关键途径，并促进合适干预策略的发现。在此基础上，我们全面概述了铁死亡相关脑损伤机制（如铁过载、氧化应激、炎症反应和占位效应）在脑出血发病机制和发展过程中的作用。脑出血后，血肿的降解和铁代谢为铁死亡提供了基本物质基础，氧化应激主要通过相关分子途径（如GPX4）参与铁死亡的脂质过氧化过程。通过综合现有证据，本文旨在为未来针对脑出血中铁死亡及相关途径的治疗策略研究提供理论基础。
