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铁死亡与肾脏疾病研究进展

Advances in Ferroptosis and Kidney Disease
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摘要 铁死亡是一种新发现的非典型的调节型细胞死亡方式,与细胞凋亡、坏死、自噬不同,其发生机制主要与铁代谢、谷光甘肽过氧化物酶4 (Glutathione Peroxidase 4, GPX4)、脂质过氧化、核因子红系2相关因子2 (Nuclear factor erythroid2-related factor 2, NRF2)、p53、铁死亡抑制蛋白1、电压依赖性阴离子通道等因素密切相关。最近有研究发现,铁死亡与急性肾损伤、肾脏纤维化等肾脏相关疾病的发生发展过程密切相关。本文主要探讨铁死亡机制研究进展及其与急性肾损伤、肾脏纤维化、糖尿病肾脏病和肾细胞癌相关机制,以期为临床上治疗肾脏病提供新方法。 Ferroptosis is a newly discovered atypical mode of regulated cell death, which distincts from apop-tosis, necrosis and autophagy. Its mechanism is mainly related to iron metabolism, Glutathione pe-roxidase 4 (GPX4), lipid peroxidation, nuclear factor erythroid2-related factor 2 (NRF2), p53, fer-roptosis inhibitory protein 1, voltage-dependent anion channel and other factors. Recently, it has been shown that iron depletion is closely linked to the course of kidney diseases such as acute kid-ney injury and renal fibrosis. This article mainly discusses the research progress of ferroptosis and its related mechanisms with acute kidney injury, renal fibrosis, diabetic nephropathy and renal cell carcinoma, in order to provide a new method for the clinical treatment of kidney disease.
出处 《临床医学进展》 2023年第12期20317-20323,共7页 Advances in Clinical Medicine
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