A Deep Insight into Ferroptosis in Renal Disease: Facts and Perspectives.

IF 4.3 3区材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC ACS Applied Electronic Materials Pub Date : 2024-03-08 eCollection Date: 2024-06-01 DOI:10.1159/000538106

Zhongyu Han, Yuanke Luo, Haoran Chen, Guochen Zhang, Luling You, Meiqi Zhang, Yumeng Lin, Lan Yuan, Shiyi Zhou

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Abstract

Background: Ferroptosis, a newly recognized form of programmed cell death, is distinguished by its reliance on reactive oxygen species and iron-mediated lipid peroxidation, setting it apart from established types like apoptosis, cell necrosis, and autophagy. Recent studies suggest its role in exacerbating or mitigating diseases by influencing metabolic and signaling pathways in conditions such as tumors and ischemic organ damage. Evidence also links ferroptosis to various kidney diseases, prompting a review of its research status and potential breakthroughs in understanding and treating these conditions.

Summary: In acute kidney disease (AKI), ferroptosis has been confirmed in animal kidneys after being induced by various factors such as renal ischemia-reperfusion and cisplatin, and glutathione peroxidase 4 (GPX4) is linked with AKI. Ferroptosis is associated with renal fibrosis in chronic kidney disease (CKD), TGF-β1 being crucial in this regard. In diabetic nephropathy (DN), high SLC7A11 and low nuclear receptor coactivator 4 (NCOA4) expressions are linked to disease progression. For polycystic kidney disease (PKD), ferroptosis promotes the disease by regulating ferroptosis in kidney tissue. Renal cell carcinoma (RCC) and lupus nephritis (LN) also have links to ferroptosis, with mtDNA and iron accumulation causing RCC and oxidative stress causing LN.

Key messages: Ferroptosis is a newly identified form of programmed cell death that is associated with various diseases. It targets metabolic and signaling pathways and has been linked to kidney diseases such as AKI, CKD, PKD, DN, LN, and clear cell RCC. Understanding its role in these diseases could lead to breakthroughs in their pathogenesis, etiology, and treatment.

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深入了解肾病中的铁蛋白沉积症：事实与观点。

背景：铁凋亡是一种新认识到的程序性细胞死亡形式，其特点是依赖活性氧和铁介导的脂质过氧化，使其有别于细胞凋亡、细胞坏死和自噬等既定类型。最近的研究表明，它通过影响肿瘤和缺血性器官损伤等情况下的代谢和信号通路，在加重或减轻疾病方面发挥作用。摘要：在急性肾脏病（AKI）中，经肾脏缺血再灌注和顺铂等多种因素诱导后，动物肾脏中的铁变态反应已被证实，谷胱甘肽过氧化物酶 4 (GPX4) 与 AKI 有关。铁蛋白沉积与慢性肾病（CKD）中的肾纤维化有关，而 TGF-β1 在这方面起着关键作用。在糖尿病肾病（DN）中，SLC7A11的高表达和核受体辅激活剂4（NCOA4）的低表达与疾病进展有关。对于多囊肾病（PKD），肾组织中的铁蛋白沉积会促进疾病的发生。肾细胞癌（RCC）和狼疮性肾炎（LN）也与高铁血症有关，mtDNA和铁积累导致RCC，氧化应激导致LN：铁凋亡是一种新发现的程序性细胞死亡形式，与多种疾病相关。它以新陈代谢和信号通路为目标，与肾脏疾病（如 AKI、CKD、PKD、DN、LN 和透明细胞 RCC）有关。了解它在这些疾病中的作用可能会在发病机制、病因学和治疗方面带来突破。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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