Mouse models for human hyperuricaemia: a critical review

被引:132
作者
Lu, Jie [1 ,2 ]
Dalbeth, Nicola [3 ]
Yin, Huiyong [4 ]
Li, Changgui [2 ]
Merriman, Tony R. [5 ]
Wei, Wen-Hua [1 ]
机构
[1] Univ Otago, Dept Womens & Childrens Hlth, Dunedin, New Zealand
[2] Qingdao Univ, Affiliated Hosp, Inst Metab Dis, Shandong Prov Key Lab Metab Dis,Dept Endocrinol &, Qingdao, Shandong, Peoples R China
[3] Univ Auckland, Dept Med, Auckland, New Zealand
[4] Chinese Acad Sci, Key Lab Nutr Metab & Food Safety, Shanghai Inst Nutr & Hlth, SIBS, Shanghai, Peoples R China
[5] Univ Otago, Dept Biochem, Dunedin, New Zealand
关键词
SERUM URIC-ACID; OXONATE-INDUCED HYPERURICEMIA; XANTHINE-OXIDASE INHIBITOR; URATE-OXIDASE; PRIMATE EVOLUTION; OXIDATIVE STRESS; KIDNEY-FUNCTION; GOUT; MICE; INFLAMMATION;
D O I
10.1038/s41584-019-0222-x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Hyperuricaemia (increased serum urate concentration) occurs mainly in higher primates, including in humans, because of inactivation of the gene encoding uricase during primate evolution. Individuals with hyperuricaemia might develop gout - a painful inflammatory arthritis caused by monosodium urate crystal deposition in articular structures. Hyperuricaemia is also associated with common chronic diseases, including hypertension, chronic kidney disease, type 2 diabetes and cardiovascular disease. Many mouse models have been developed to investigate the causal mechanisms for hyperuricaemia. These models are highly diverse and can be divided into two broad categories: mice with genetic modifications (genetically induced models) and mice exposed to certain environmental factors (environmentally induced models; for example, pharmaceutical or dietary induction). This Review provides an overview of the mouse models of hyperuricaemia and the relevance of these models to human hyperuricaemia, with an emphasis on those models generated through genetic modifications. The challenges in developing and comparing mouse models of hyperuricaemia and future research directions are also outlined.
引用
收藏
页码:413 / 426
页数:14
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