自溶性坏死是一种经过调节的细胞死亡过程，主要表现为铁依赖性脂质过氧化物的积累。自溶性坏死的主要原因是胞内氧化系统（例如LOXs，POR，ROS）和抗氧化系统（例如GSH / GPx4，CoQ10 / FSP1，BH4 / GCH1）的失衡，该失衡通过一个复杂的网络进行调节。在过去的十年中，这个代谢网络不断得到改进，并且与各种病理生理过程的联系也逐渐建立起来。凋亡长期以来一直被视为经过调节的细胞死亡的唯一形式，化疗药物应用于诱导癌细胞凋亡是主流方法。然而，研究表明癌细胞的关键特征是对凋亡和化疗药物的抵抗力。高增殖的癌细胞常常具有非常活跃的脂质代谢和铁代谢，为自溶性坏死铺平了道路。有趣的是，研究人员发现，耐药或高度侵袭性的癌细胞更容易发生自溶性坏死。因此，自溶性坏死可能是一种消灭癌细胞的潜在策略。此外，还发现了自溶性坏死与其他疾病之间的联系，例如神经系统疾病和缺血再灌注损伤。从自溶性坏死的角度理解这些疾病可能为临床治疗提供新的见解。本文回顾了自溶性坏死中的代谢过程，并总结了不同疾病中自溶性坏死的潜在机制和靶点。©2022年作者，独家授权给Springer Nature B.V。

Ferroptosis is a regulated cell death mainly manifested by iron-dependent lipid peroxide accumulation. The leading cause of ferroptosis is the imbalance of intracellular oxidative systems (e.g., LOXs, POR, ROS) and antioxidant systems (e.g., GSH/GPx4, CoQ10/FSP1, BH4/GCH1), which is regulated by a complex network. In the past decade, this metabolic network has been continuously refined, and the links with various pathophysiological processes have been gradually established. Apoptosis has been regarded as the only form of regulated cell death for a long time, and the application of chemotherapeutic drugs to induce apoptosis of cancer cells is the mainstream method. However, studies have reported that cancer cells' key features are resistance to apoptosis and chemotherapeutics. For high proliferation, cancer cells often have very active lipid metabolism and iron metabolism, which pave the way for ferroptosis. Interestingly, researchers found that drug-resistant or highly aggressive cancer cells are more prone to ferroptosis. Therefore, ferroptosis may be a potential strategy to eliminate cancer cells. In addition, links between ferroptosis and other diseases, such as neurological disorders and ischemia-reperfusion injury, have also been found. Understanding these diseases from the perspective of ferroptosis may provide new insights into clinical treatment. Herein, the metabolic processes in ferroptosis are reviewed, and the potential mechanisms and targets of ferroptosis in different diseases are summarized.© 2022. The Author(s), under exclusive licence to Springer Nature B.V.