Huang Sijia, Liu Kexin, Su Ying, Wang Feng, Feng Tao
Department of Ophthalmology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, China.
Eye Hospital, The First Affiliated Hospital Harbin Medical University, Harbin, 150001, China.
Mol Cell Biochem. 2023 Apr;478(4):721-727. doi: 10.1007/s11010-022-04545-7. Epub 2022 Sep 2.
Unlike other death forms, such as autophagy, necrosis, and apoptosis, ferroptosis is a novel type of programmed cell death with iron-dependent properties. Esteroxygenase affects the content of unsaturated fatty acids and promotes lipid peroxidation. In addition, GSH can cause the reduction of GPX4, which can cause ferroptosis. P53 and its signaling pathways also regulate ferroptosis. Recent studies have confirmed that ferroptosis also promotes the death of RGC. The progressive loss of RGC is one of the pathological features of glaucoma, indicating that ferroptosis may be related to the onset of glaucoma. Down-regulation of GPX4 leads to the loss of nerve cells, which suggests that ferroptosis may also be related to diseases related to optic nerve damage. At present, ferroptosis has been extensively researched and advanced in systemic diseases, such as cardiovascular diseases, gastrointestinal tumors such as stomach, liver, and pancreas, and brain diseases. This review focuses on the research progress of ferroptosis in ophthalmic diseases, especially glaucoma and optic nerve damage.
与其他死亡形式，如自噬、坏死和凋亡不同，铁死亡是一种新型的程序性细胞死亡，具有铁依赖性。酯氧合酶影响不饱和脂肪酸的含量并促进脂质过氧化。此外，谷胱甘肽（GSH）可导致谷胱甘肽过氧化物酶4（GPX4）减少，从而引发铁死亡。P53及其信号通路也调节铁死亡。最近的研究证实，铁死亡也会促进视网膜神经节细胞（RGC）的死亡。RGC的渐进性丧失是青光眼的病理特征之一，表明铁死亡可能与青光眼的发病有关。GPX4的下调会导致神经细胞的丧失，这表明铁死亡也可能与视神经损伤相关疾病有关。目前，铁死亡在全身性疾病，如心血管疾病、胃肠道肿瘤（如胃癌、肝癌和胰腺癌）以及脑部疾病中已得到广泛研究并取得进展。本综述重点关注铁死亡在眼科疾病，尤其是青光眼和视神经损伤方面的研究进展。
