急性肾损伤(AKI)是公共卫生中的一个重要问题。显示出较高的发生率和死亡率。Ferroptosis,一种形式的程序性细胞死亡(PCD),其特征是铁积累和增强的脂质过氧化。最近的研究已经证明了铁性凋亡在不同刺激引起的AKI中的重要意义。包括缺血再灌注损伤(IRI),败血症和毒素。自噬,针对受损的细胞器和大分子进行降解和回收的多步骤过程,在AKI中也起着至关重要的作用。前期研究表明近端小管自噬缺失可加重肾小管损伤和肾功能丧失,表明自噬在AKI中的保护作用。因此,寻找刺激自噬的方法已成为重要的治疗策略。选择性自噬在影响铁凋亡中的作用的最新发现已经确定了AKI的新治疗靶标,并强调了理解自噬和铁凋亡之间的串扰的重要性。本研究旨在对参与铁凋亡和自噬的信号通路进行综述,重点介绍选择性自噬和自噬依赖性铁凋亡的机制和功能。我们希望为将来研究AKI以及其他疾病中自噬与铁凋亡之间的相互作用奠定基础。
Acute kidney injury (AKI) is a significant issue in public health, displaying a high occurrence rate and mortality rate. Ferroptosis, a form of programmed cell death (PCD), is characterized by iron accumulation and intensified lipid peroxidation. Recent studies have demonstrated the pivotal significance of ferroptosis in AKI caused by diverse stimuli, including ischemia-reperfusion injury (IRI), sepsis and toxins. Autophagy, a multistep process that targets damaged organelles and macromolecules for degradation and recycling, also plays an essential role in AKI. Previous research has demonstrated that autophagy deletion in proximal tubules could aggravate tubular injury and renal function loss, indicating the protective function of autophagy in AKI. Consequently, finding ways to stimulate autophagy has become a crucial therapeutic strategy. The recent discovery of the role of selective autophagy in influencing ferroptosis has identified new therapeutic targets for AKI and has highlighted the importance of understanding the cross-talk between autophagy and ferroptosis. This study aims to provide an overview of the signaling pathways involved in ferroptosis and autophagy, focusing on the mechanisms and functions of selective autophagy and autophagy-dependent ferroptosis. We hope to establish a foundation for future investigations into the interaction between autophagy and ferroptosis in AKI as well as other diseases.