脱铁性贫血在急性肺损伤中的作用及机制。

IF 3.4 3区 生物学 Q3 CELL BIOLOGY Cell Cycle Pub Date : 2023-10-01 Epub Date: 2023-12-05 DOI:10.1080/15384101.2023.2278328
Tingting Yu, Shibo Sun
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引用次数: 0

摘要

脱铁症是一种新的非凋亡细胞死亡,由铁代谢失调、氨基酸或脂质过氧化引起。越来越多的研究表明,脱铁性贫血与急性肺损伤有关。本文旨在综述脱铁性贫血在急性肺损伤中的作用。ALI是一种常见的呼吸道疾病,死亡率很高。抑制肺细胞脱铁改善ALI。此外,一些信号通路与ALI中的脱铁性贫血有关,涉及铁稳态、脂质过氧化和氨基酸代谢。此外,还有多种关键因素调节ALI中脱铁性贫血的发生,如ACSL4、NRF2和P53。ACSL4可促进ALI患者的铁蛋白脱失,而NRF2可减轻ALI患者铁蛋白脱脱。P53的主要作用是促进脱铁性贫血。因此,脱铁性贫血与ALI有关,可能是ALI的重要治疗靶点。
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Role and mechanism of ferroptosis in acute lung injury.

Ferroptosis is a new non-apoptotic cell death caused by the accumulation of dysregulated metabolism of ferric iron, amino acids or lipid peroxidation. Increasing studies suggest that ferroptosis is involved in the acute lung injury (ALI). This article aims to review the role of ferroptosis in ALI. ALI is a common respiratory disease and presents a high mortality rate. Inhibiting cell ferroptosis of lung improves the ALI. In addition, several signaling pathways are related to ferroptosis in ALI, involving in iron homeostasis, lipid peroxidation, and amino acid metabolism. Moreover, there are various key factors to regulate the occurrence of ferroptosis in ALI, such as ACSL4, NRF2, and P53. The ACSL4 promotes the ferroptosis, while the NRF2 alleviates the ferroptosis in ALI. The main effect of P53 is to promote ferroptosis. Accordingly, ferroptosis is involved in ALI and may be an important therapeutic target for ALI.

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来源期刊
Cell Cycle
Cell Cycle 生物-细胞生物学
CiteScore
7.70
自引率
2.30%
发文量
281
审稿时长
1 months
期刊介绍: Cell Cycle is a bi-weekly peer-reviewed journal of high priority research from all areas of cell biology. Cell Cycle covers all topics from yeast to man, from DNA to function, from development to aging, from stem cells to cell senescence, from metabolism to cell death, from cancer to neurobiology, from molecular biology to therapeutics. Our goal is fast publication of outstanding research.
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