ABCG2 dysfunction causes hyperuricemia due to both renal urate underexcretion and renal urate overload.

ABCG2 dysfunction causes hyperuricemia due to both renal urate underexcretion and renal urate overload.
复制标题

DOI:
10.1038/srep03755
复制
发表时间:
2014-01-20
期刊:
影响因子:
4.6
通讯作者:
Shinomiya N
Shinomiya N
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Matsuo H;Nakayama A;Sakiyama M;Chiba T;Shimizu S;Kawamura Y;Nakashima H;Nakamura T;Takada Y;Oikawa Y;Takada T;Nakaoka H;Abe J;Inoue H;Wakai K;Kawai S;Guang Y;Nakagawa H;Ito T;Niwa K;Yamamoto K;Sakurai Y;Suzuki H;Hosoya T;Ichida K;Shimizu T;Shinomiya N

文献摘要

参考文献

被引文献

相似文献

痛风是一种常见病,是由高尿酸血症引起的。我们已经报道了尿酸输出蛋白ABCG 2功能障碍是肾超负荷(ROL)高尿酸血症的主要原因,但其与最常见的肾排泄不足(芸香)高尿酸血症的关系至今尚未明确。在这项研究中,对644名日本男性高尿酸血症患者和1,623名对照者进行的关联分析显示,根据损伤的严重程度,ABCG 2功能障碍显著增加了芸香高尿酸血症以及总体和ROL高尿酸血症的风险。ABCG 2功能障碍引起肾脏尿酸盐排泄不足,并诱发高尿酸血症,即使肾脏尿酸盐超负荷并不显著。这些结果表明,ABCG 2在肾脏和肾外尿酸排泄机制中起着重要的生理作用。我们的研究结果表明ABCG 2作为高尿酸血症和痛风的有前途的治疗和筛选靶点的重要性。
Gout is a common disease which results from hyperuricemia. We have reported that the dysfunction of urate exporter ABCG2 is the major cause of renal overload (ROL) hyperuricemia, but its involvement in renal underexcretion (RUE) hyperuricemia, the most prevalent subtype, is not clearly explained so far. In this study, the association analysis with 644 hyperuricemia patients and 1,623 controls in male Japanese revealed that ABCG2 dysfunction significantly increased the risk of RUE hyperuricemia as well as overall and ROL hyperuricemia, according to the severity of impairment. ABCG2 dysfunction caused renal urate underexcretion and induced hyperuricemia even if the renal urate overload was not remarkable. These results show that ABCG2 plays physiologically important roles in both renal and extra-renal urate excretion mechanisms. Our findings indicate the importance of ABCG2 as a promising therapeutic and screening target of hyperuricemia and gout.
DOI: 10.1038/srep02014
发表时间: 2013
期刊: Scientific reports
影响因子: 4.6
作者:
Matsuo H;Ichida K;Takada T;Nakayama A;Nakashima H;Nakamura T;Kawamura Y;Takada Y;Yamamoto K;Inoue H;Oikawa Y;Naito M;Hishida A;Wakai K;Okada C;Shimizu S;Sakiyama M;Chiba T;Ogata H;Niwa K;Hosoyamada M;Mori A;Hamajima N;Suzuki H;Kanai Y;Sakurai Y;Hosoya T;Shimizu T;Shinomiya N
通讯作者: Shinomiya N
DOI: 10.1038/ncomms1756
发表时间: 2012-04-03
影响因子: 16.6
作者:
通讯作者: --
DOI: 10.2353/jmoldx.2008.070111
发表时间: 2008-03-01
影响因子: 4.1
作者:
Margraf, Rebecca L.;Mao, Rong;Wittwer, Carl T.
通讯作者: Wittwer, Carl T.
DOI: 10.1038/nature742
发表时间: 2002-05-23
期刊: NATURE
影响因子: 64.8
作者:
Enomoto, A;Kimura, H;Endou, H
通讯作者: Endou, H
DOI: 10.1007/s13577-013-0073-8
发表时间: 2013-12
期刊: HUMAN CELL
影响因子: 4.3
作者:
Nakayama, Akiyoshi;Matsuo, Hirotaka;Shimizu, Takuya;Ogata, Hiraku;Takada, Yuzo;Nakashima, Hiroshi;Nakamura, Takahiro;Shimizu, Seiko;Chiba, Toshinori;Sakiyama, Masayuki;Ushiyama, Chisaki;Takada, Tappei;Inoue, Katsuhisa;Kawai, Sayo;Hishida, Asahi;Wakai, Kenji;Hamajima, Nobuyuki;Ichida, Kimiyoshi;Sakurai, Yutaka;Kato, Yukio;Shimizu, Toru;Shinomiya, Nariyoshi
通讯作者: Shinomiya, Nariyoshi