An update of genetics, co-morbidities and management of hyperuricaemia

被引：12

作者：

Zhu, Chunsheng ^{[1
]}

Sun, Bao ^{[2
,3
]}

Zhang, Bing ^{[4
]}

Zhou, Zheng ^{[1
]}

机构：

[1] Zhengzhou Univ, Affiliated Hosp 1, Zhengzhou, Peoples R China

[2] Cent South Univ, Xiangya Hosp 2, Dept Pharm, Changsha, Peoples R China

[3] Cent South Univ, Inst Clin Pharmacol, Changsha, Peoples R China

[4] Beijing Univ Chinese Med, Sch Chinese Pharm, Beijing, Peoples R China

来源：

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY | 2021年 / 48卷 / 10期

关键词：

co-morbidities; hyperuricaemia; oxidative stress; transporters; urate-lowering therapy; uric acid; URIC-ACID LEVELS; CHRONIC KIDNEY-DISEASE; URATE TRANSPORTER; ENDOTHELIAL DYSFUNCTION; CARDIOVASCULAR-DISEASE; FUNCTIONAL-ANALYSIS; ALLELIC VARIANTS; SYSTEMS BIOLOGY; COMMON VARIANT; GOUT;

D O I：

10.1111/1440-1681.13539

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Hyperuricaemia (HU) caused by disorders of purine metabolism is a metabolic disease. A number of epidemiological reports have confirmed that HU is correlated with multiple disorders, such as chronic kidney diseases, cardiovascular disease and gout. Recent studies showed that the expression and functional changes of uric acid transporters, including URAT1, GLUT9 and ABCG2, were associated with HU. Moreover, a large number of genome-wide association studies have shown that these transporters' dysfunction leads to HU. In this review, we describe the recent progress of aetiology and related transporters of HU, and we also summarise the common co-morbidities possible mechanisms, as well as the potential pharmacological and non-pharmacological treatment methods for HU, aiming to provide new ideas for the treatment of HU.

引用

页码：1305 / 1316

页数：12

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