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

0 UROLOGY & NEPHROLOGY
Tanima Chatterjee, Abolfazl Zarjou
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引用次数: 0

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.
探索急性肾损伤的复杂发病机制:探索巨噬细胞动力学、线粒体功能障碍和铁蛋白沉积途径
急性肾损伤是指肾功能急剧下降,同时伴有生理和体内平衡紊乱,是影响短期和长期健康的一个独立风险因素。随着全球急性肾损伤发病率的持续上升,急性肾损伤所带来的重大临床和经济挑战凸显了及时识别急性肾损伤的必要性,并需要应用新颖、前沿的策略来降低其严重程度并促进康复。了解急性肾损伤发病机制的多层面级联事件对于制定有效的预防和治疗策略至关重要。为便于深入探讨新出现的治疗靶点,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生成动力学的改变,并深入探讨铁蛋白沉积对肾损伤所起作用的分子机制。
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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来源期刊
CiteScore
5.30
自引率
0.00%
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