铁死亡是一种受调节的细胞死亡形式，其特征是铁依赖性脂质过氧化导致细胞膜氧化损伤。细胞对铁死亡的敏感性受到铁过载、脂质代谢和抗氧化系统调节等因素的影响。褪黑激素具有螯合铁、调节铁代谢蛋白、调节脂质过氧化和调节抗氧化系统的能力，有望成为介导铁死亡的潜在治疗剂。已批准的针对铁死亡的药物的可用性有限；因此，褪黑激素因其在减轻非癌症疾病中的铁死亡方面的安全性和有效性而成为广泛应用的候选者。褪黑素已被证明可以在非癌症疾病的细胞和动物模型中减轻铁死亡，并在心脏、大脑、肺、肝脏、肾脏和骨骼等器官中显示出有效性。这篇综述概述了铁死亡的分子机制，研究了褪黑激素对铁死亡的潜在影响，并讨论了褪黑激素作为治疗铁死亡相关疾病的有希望的干预措施的治疗潜力。通过这次讨论，我们的目标是为开发褪黑激素作为调节多种疾病背景下铁死亡的治疗策略奠定坚实的基础。版权所有 © 2023 Elsevier Inc. 保留所有权利。

Ferroptosis, a regulated form of cell death, is characterized by iron-dependent lipid peroxidation leading to oxidative damage to cell membranes. Cell sensitivity to ferroptosis is influenced by factors such as iron overload, lipid metabolism, and the regulation of the antioxidant system. Melatonin, with its demonstrated capacity to chelate iron, modulate iron metabolism proteins, regulate lipid peroxidation, and regulate antioxidant systems, has promise as a potential therapeutic agent in mediating ferroptosis. The availability of approved drugs targeting ferroptosis is limited; therefore, melatonin is a candidate for broad application due to its safety and efficacy in attenuating ferroptosis in noncancerous diseases. Melatonin has been demonstrated to attenuate ferroptosis in cellular and animal models of noncancerous diseases, showcasing effectiveness in organs such as the heart, brain, lung, liver, kidney, and bone. This review outlines the molecular mechanisms of ferroptosis, investigates melatonin's potential effects on ferroptosis, and discusses melatonin's therapeutic potential as a promising intervention against diseases associated with ferroptosis. Through this discourse, we aim to lay a strong foundation for developing melatonin as a therapeutic strategy to modulate ferroptosis in a variety of disease contexts.Copyright © 2023 Elsevier Inc. All rights reserved.