Role of urate transporters in the kidneys and intestine in uric acid homeostasis.

IF 2.9 3区 医学 Q1 UROLOGY & NEPHROLOGY
Su Hyun Kim, Jungho Shin, Hyung-Eun Son, Duk-Hee Kang
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引用次数: 0

Abstract

Hyperuricemia is frequently observed in patients with chronic kidney disease and is recognized as a significant contributor to the progression of renal dysfunction. On the other hand, hypouricemia, although less thoroughly studied, has been implicated in exercise-induced acute kidney injury and urolithiasis. Uric acid (UA), the final product of purine metabolism, is predominantly synthesized in the liver and excreted through both renal and intestinal pathways. The metabolism and excretion of UA are intricately linked to kidney function, underscoring their clinical significance in the context of renal disease. This review provides a comprehensive review of UA metabolism and the key urate transporters, including URAT1, GLUT9, OATs, and ABCG2, which play pivotal roles in maintaining UA homeostasis. Additionally, this review discusses the genetic and environmental factors that influence UA regulation, with a particular focus on the pathological consequences of transporter dysfunction. By elucidating the mechanisms underlying UA handling in the renal and intestinal systems, this review aims to enhance our understanding of UA-related pathophysiology, and to inform the development of targeted therapeutic strategies for modulating UA transport.

肾和肠中尿酸转运蛋白在尿酸稳态中的作用。
高尿酸血症常见于慢性肾病患者,被认为是肾功能障碍进展的重要因素。另一方面,尽管研究较少,但低尿酸血症与运动引起的急性肾损伤和尿石症有关。尿酸(UA)是嘌呤代谢的最终产物,主要在肝脏合成,并通过肾脏和肠道途径排出体外。UA的代谢和排泄与肾脏功能有着复杂的联系,强调了其在肾脏疾病中的临床意义。本文综述了UA代谢和关键的尿酸转运蛋白,包括URAT1、GLUT9、OATs和ABCG2,它们在维持UA稳态中起着关键作用。此外,本文还讨论了影响UA调节的遗传和环境因素,特别关注转运蛋白功能障碍的病理后果。通过阐明肾脏和肠道系统中UA处理的机制,本综述旨在增强我们对UA相关病理生理学的理解,并为调节UA运输的靶向治疗策略的发展提供信息。
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
4.60
自引率
10.00%
发文量
77
审稿时长
10 weeks
期刊介绍: Kidney Research and Clinical Practice (formerly The Korean Journal of Nephrology; ISSN 1975-9460, launched in 1982), the official journal of the Korean Society of Nephrology, is an international, peer-reviewed journal published in English. Its ISO abbreviation is Kidney Res Clin Pract. To provide an efficient venue for dissemination of knowledge and discussion of topics related to basic renal science and clinical practice, the journal offers open access (free submission and free access) and considers articles on all aspects of clinical nephrology and hypertension as well as related molecular genetics, anatomy, pathology, physiology, pharmacology, and immunology. In particular, the journal focuses on translational renal research that helps bridging laboratory discovery with the diagnosis and treatment of human kidney disease. Topics covered include basic science with possible clinical applicability and papers on the pathophysiological basis of disease processes of the kidney. Original researches from areas of intervention nephrology or dialysis access are also welcomed. Major article types considered for publication include original research and reviews on current topics of interest. Accepted manuscripts are granted free online open-access immediately after publication, which permits its users to read, download, copy, distribute, print, search, or link to the full texts of its articles to facilitate access to a broad readership. Circulation number of print copies is 1,600.
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