Department of Food Nutrition and Safety, Dalian Medical University, No. 9W. Lushun South Road, Dalian 116044, China.
Department of Cardiology, the First Affiliated Hospital of Dalian Medical University, Dalian 116011, China.
Pathol Res Pract. 2024 Oct;262:155553. doi: 10.1016/j.prp.2024.155553. Epub 2024 Aug 22.
Ferritinophagy is a regulatory pathway of iron homeostasis. It is a process in which nuclear receptor coactivator 4 (NCOA4) carries ferritin to autophagolysosomes for degradation. After ferritin is degraded by autophagy, iron ions are released, which promotes the labile iron pool (LIP) to drive the Fenton reaction to cause lipid peroxidation. Furthermore, ferroptosis promoted by the accumulation of lipid reactive oxygen species (ROS) induced by ferritinophagy can cause a variety of systemic diseases. In clinical studies, targeting the genes regulating ferritinophagy can prevent and treat such diseases. This article describes the key regulatory factors of ferritinophagy and the mechanism of ferritinophagy involved in ferroptosis. It also reviews the damage of ferritinophagy to the body, providing a theoretical basis for further finding clinical treatment methods.
铁蛋白自噬是铁稳态的调节途径。它是一个过程，其中核受体共激活因子 4（NCOA4）将铁蛋白携带到自噬溶酶体进行降解。铁蛋白被自噬降解后，铁离子被释放，促进不稳定铁池（LIP）驱动芬顿反应引起脂质过氧化。此外，铁蛋白自噬诱导的脂质活性氧（ROS）积累促进的铁死亡会导致多种全身性疾病。在临床研究中，针对调节铁蛋白自噬的基因可以预防和治疗这些疾病。本文描述了铁蛋白自噬的关键调节因子和涉及铁死亡的铁蛋白自噬机制，并回顾了铁蛋白自噬对机体的损害，为进一步寻找临床治疗方法提供了理论依据。
