粒体自噬
线粒体
氧化应激
程序性细胞死亡
细胞生物学
急性肾损伤
活性氧
平衡
信号转导
肾
癌症研究
生物
化学
细胞凋亡
自噬
医学
生物化学
内科学
内分泌学
作者
Wenju Li,Zhangmin Xiang,Yufei Xing,Li Shen,Shaolin Shi
标识
DOI:10.1038/s41419-022-04770-4
摘要
Ferroptosis, a form of regulated cell death, plays an important role in acute kidney injury (AKI). Previous studies have shown that prolyl hydroxylase domain protein (PHD) inhibitors that activate HIF signaling provide strong protection against AKI, which is characterized by marked cell death. However, the relationship between PHD inhibition/HIF signaling and ferroptosis in AKI has not been elucidated. Here, we review recent studies to explore the issue. First, we will review the literature concerning the functions of HIF in promoting mitophagy, suppressing mitochondrial respiration and modulating redox homeostasis. Second, we will describe the current understanding of ferroptosis and its role in AKI, particularly from the perspective of mitochondrial dysfunction. Finally, we will discuss the possibility that mitochondria link PHD inhibition/HIF signaling and ferroptosis in AKI. In conclusion, we propose that HIF may protect renal cells against ferroptosis in AKI by reducing mitochondrial oxidative stress and damage.
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