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An update of genetics, co‐morbidities and management of hyperuricaemia
Author(s) -
Zhu Chunsheng,
Sun Bao,
Zhang Bing,
Zhou Zheng
Publication year - 2021
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.13539
Subject(s) - gout , disease , uric acid , hyperuricemia , medicine , transporter , bioinformatics , purine , etiology , biology , genetics , gene , biochemistry , enzyme
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.