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探索急性肾损伤的复杂发病机制:探究巨噬细胞动态变化、线粒体功能障碍和铁死亡途径

Navigating the Complex Pathogenesis of Acute Kidney Injury: Exploring Macrophage Dynamics, Mitochondrial Dysfunction, and Ferroptosis Pathways.

作者信息

Chatterjee Tanima, Zarjou Abolfazl

机构信息

Department of Medicine, University of Alabama at Birmingham, Birmingham, AL.

Department of Medicine, University of Alabama at Birmingham, Birmingham, AL.

出版信息

Adv Kidney Dis Health. 2025 Mar;32(2):122-132. doi: 10.1053/j.akdh.2024.12.004.

DOI:10.1053/j.akdh.2024.12.004
PMID:40222799
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11999248/
Abstract

Acute kidney injury, a rapid decline in kidney function coupled with physiological and homeostatic perturbations, is an independent risk factor for both short-term and long-term health outcomes. As incidence of acute kidney injury continues to rise globally, the significant clinical and economic challenge of acute kidney injury underscores the need for its prompt recognition and application of novel and germane strategies to reduce its severity and facilitate recovery. Understanding the multifaceted cascade of events engaged in pathogenesis of acute kidney injury is pivotal for the development of effective preventive and therapeutic strategies. To facilitate an in-depth discussion on emerging therapeutic targets, this review will examine the role of macrophages in kidney injury and repair, explore the alterations in mitochondrial biogenesis dynamics induced by acute kidney injury, and provide insights into the molecular mechanisms underlying the contribution of ferroptosis to kidney injury.

摘要

急性肾损伤是指肾功能迅速下降并伴有生理和内环境稳态紊乱,它是短期和长期健康结局的独立危险因素。随着全球急性肾损伤的发病率持续上升,急性肾损伤带来的重大临床和经济挑战凸显了迅速识别并应用新颖且相关策略以降低其严重程度并促进恢复的必要性。了解参与急性肾损伤发病机制的多方面事件级联对于制定有效的预防和治疗策略至关重要。为便于深入讨论新兴治疗靶点,本综述将研究巨噬细胞在肾损伤和修复中的作用,探讨急性肾损伤诱导的线粒体生物发生动力学变化,并深入了解铁死亡对肾损伤作用的分子机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dedd/11999248/79f8daf30a55/nihms-2043763-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dedd/11999248/79f8daf30a55/nihms-2043763-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dedd/11999248/79f8daf30a55/nihms-2043763-f0001.jpg

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本文引用的文献

1
GPX4, ferroptosis, and diseases.GPX4、铁死亡与疾病。
Biomed Pharmacother. 2024 May;174:116512. doi: 10.1016/j.biopha.2024.116512. Epub 2024 Apr 3.
2
Distinct developmental reprogramming footprint of macrophages during acute kidney injury across species.跨物种急性肾损伤期间巨噬细胞独特的发育重编程印记
Am J Physiol Renal Physiol. 2024 Apr 1;326(4):F635-F641. doi: 10.1152/ajprenal.00013.2024. Epub 2024 Feb 15.
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Role of ferroptosis in chronic kidney disease.铁死亡在慢性肾脏病中的作用。
Cell Commun Signal. 2024 Feb 12;22(1):113. doi: 10.1186/s12964-023-01422-8.
4
The mechanism of ferroptosis and its related diseases.铁死亡的机制及其相关疾病。
Mol Biomed. 2023 Oct 16;4(1):33. doi: 10.1186/s43556-023-00142-2.
5
NRF2, a Superstar of Ferroptosis.NRF2,铁死亡的明星分子。
Antioxidants (Basel). 2023 Sep 8;12(9):1739. doi: 10.3390/antiox12091739.
6
Mitochondrial dynamics in health and disease: mechanisms and potential targets.线粒体动态平衡在健康和疾病中的作用:机制与潜在靶点
Signal Transduct Target Ther. 2023 Sep 6;8(1):333. doi: 10.1038/s41392-023-01547-9.
7
The Road from AKI to CKD: Molecular Mechanisms and Therapeutic Targets of Ferroptosis.从急性肾损伤到慢性肾脏病:铁死亡的分子机制和治疗靶点。
Cell Death Dis. 2023 Jul 13;14(7):426. doi: 10.1038/s41419-023-05969-9.
8
Mitochondrial dynamics involves molecular and mechanical events in motility, fusion and fission.线粒体动力学涉及运动、融合和裂变中的分子及机械事件。
Front Cell Dev Biol. 2022 Oct 19;10:1010232. doi: 10.3389/fcell.2022.1010232. eCollection 2022.
9
Mitochondrial Fission and Fusion: Molecular Mechanisms, Biological Functions, and Related Disorders.线粒体分裂与融合:分子机制、生物学功能及相关疾病
Membranes (Basel). 2022 Sep 16;12(9):893. doi: 10.3390/membranes12090893.
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System X /GSH/GPX4 : An important antioxidant system for the ferroptosis in drug-resistant solid tumor therapy.系统X/谷胱甘肽/谷胱甘肽过氧化物酶4:耐药实体瘤治疗中细胞铁死亡的重要抗氧化系统。
Front Pharmacol. 2022 Aug 29;13:910292. doi: 10.3389/fphar.2022.910292. eCollection 2022.