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谷胱甘肽过氧化物酶4（Gpx4）与铁死亡：它有何特别之处？

Glutathione peroxidase 4 (Gpx4) and ferroptosis: what's so special about it?

作者信息

Conrad Marcus, Friedmann Angeli José Pedro

机构信息

Institute of Developmental Genetics; Helmholtz Zentrum München; , München, Germany.

出版信息

Mol Cell Oncol. 2015 Jan 30;2(3):e995047. doi: 10.4161/23723556.2014.995047. eCollection 2015 Jul-Sep.

DOI:10.4161/23723556.2014.995047
PMID:27308484
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4905320/
Abstract

The system XC (-)/glutathione/glutathione peroxidase 4 (Gpx4) axis pivotally controls ferroptosis, a recently described form of regulated non-apoptotic cell death. Compelling evidence has established that this route of cell death is not only of high relevance for triggering cancer cell death, but also proves to be amenable for therapeutic intervention to halt ischemia/reperfusion-related diseases.

摘要

系统XC（-）/谷胱甘肽/谷胱甘肽过氧化物酶4（Gpx4）轴对铁死亡起着关键的调控作用，铁死亡是一种最近被描述的受调控的非凋亡性细胞死亡形式。有力的证据表明，这种细胞死亡途径不仅与触发癌细胞死亡高度相关，而且还被证明可用于治疗干预以阻止缺血/再灌注相关疾病。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8fd8/4905320/92e2310a0a83/kmco-02-03-995047-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8fd8/4905320/92e2310a0a83/kmco-02-03-995047-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8fd8/4905320/92e2310a0a83/kmco-02-03-995047-g001.jpg

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Synchronized renal tubular cell death involves ferroptosis.同步性肾小管细胞死亡涉及铁死亡。
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Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS.琥珀酸的缺血性积累通过线粒体活性氧控制再灌注损伤。
Antioxidants (Basel). 2025 Apr 28;14(5):527. doi: 10.3390/antiox14050527.
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Int J Mol Sci. 2025 Mar 23;26(7):2915. doi: 10.3390/ijms26072915.
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