Ferroptosis is an iron- and lipotoxicity-dependent form of regulated cell death (RCD). It is morphologically and biochemically distinct from characteristics of other cell death. This modality has been intensively investigated in recent years due to its involvement in a wide array of pathologies, including cancer, neurodegenerative diseases, and acute kidney injury. Dysregulation of ferroptosis has also been linked to various liver diseases and its modification may provide a hopeful and attractive therapeutic concept. Indeed, targeting ferroptosis may prevent the pathophysiological progression of several liver diseases, such as hemochromatosis, nonalcoholic steatohepatitis, and ethanol-induced liver injury. On the contrary, enhancing ferroptosis may promote sorafenib-induced ferroptosis and pave the way for combination therapy in hepatocellular carcinoma. Glutathione peroxidase 4 (GPx4) and system x_c⁻ have been identified as key players to mediate ferroptosis pathway. More recently diverse signaling pathways have also been observed. The connection between ferroptosis and other forms of RCD is intricate and compelling, where discoveries in this field advance our understanding of cell survival and fate. In this review, we summarize the central molecular machinery of ferroptosis, describe the role of ferroptosis in non-cancer hepatic disease conditions and discuss the potential to manipulate ferroptosis as a therapeutic strategy.

Ferroptosis是铁和脂毒性依赖性形式的受调节细胞死亡（RCD）。在形态和生化上与其他细胞死亡特征不同。近年来，由于这种方式涉及多种病理学，包括癌症，神经退行性疾病和急性肾损伤，对此进行了深入研究。肥大症的失调也与各种肝脏疾病有关，其改变可能提供一种有希望和有吸引力的治疗概念。的确，针对肥大症可以预防几种肝脏疾病的病理生理进展，例如血色素沉着症，非酒精性脂肪性肝炎和乙醇引起的肝损伤。反之，增强肥大症可能促进索拉非尼诱导的肥大症，并为肝细胞癌的联合治疗铺平道路。谷胱甘肽过氧化物酶4（GPx4）和系统x_Ç ^-已被确定为关键球员调解ferroptosis途径。最近还观察到多种信号传导途径。肥大病和其他形式的RCD之间的联系错综复杂且令人信服，在该领域的发现使我们对细胞存活和命运有了更深入的了解。在这篇综述中，我们总结了肥大症的主要分子机制，描述了肥大症在非癌性肝病中的作用，并讨论了将肥大症作为治疗策略的潜力。