自噬与铁死亡——有何关联？
Autophagy and Ferroptosis - What's the Connection?
作者信息
Kang Rui, Tang Daolin
机构信息
Department of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania 15213, USA.
The Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong 510150, China.
出版信息
Curr Pathobiol Rep. 2017 Jun;5(2):153-159. doi: 10.1007/s40139-017-0139-5. Epub 2017 Apr 20.
PURPOSE OF REVIEW
Autophagy is a conserved intracellular degradation system and plays a dual role in cell death, depending on context and phase. Ferroptosis is a new form of regulated cell death that mainly depends on iron accumulation and lipid peroxidation. In this review, we summarize the processes of autophagy and ferroptosis and discuss their crosstalk mechanisms at the molecular level.
RECENT FINDINGS
The original study shows that ferroptosis is morphologically, biochemically, and genetically distinct from autophagy and other types of cell death. However, recent studies demonstrate that activation of ferroptosis is indeed dependent on the induction of autophagy. Additionally, many ferroptosis regulators such as SLC7A11, GPX4, NRF2, p53, HSPB1, CISD1, FANCD2, and ACSL4 have been identified as potential regulators of autophagy.
SUMMARY
This review not only highlights the importance of autophagy as an emerging mechanism of ferroptosis, but also raises new insights regarding regulated cell death.
综述目的
自噬是一种保守的细胞内降解系统，在细胞死亡中发挥双重作用，这取决于具体情况和阶段。铁死亡是一种新的程序性细胞死亡形式，主要依赖于铁的积累和脂质过氧化。在本综述中，我们总结了自噬和铁死亡的过程，并在分子水平上讨论了它们的相互作用机制。
最新发现
最初的研究表明，铁死亡在形态、生化和基因方面与自噬及其他类型的细胞死亡不同。然而，最近的研究表明，铁死亡的激活确实依赖于自噬的诱导。此外，许多铁死亡调节因子，如SLC7A11、GPX4、NRF2、p53、HSPB1、CISD1、FANCD2和ACSL4已被确定为自噬的潜在调节因子。
总结
本综述不仅强调了自噬作为铁死亡新机制的重要性，还对程序性细胞死亡提出了新的见解。
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