The long noncoding RNA Tug1 connects metabolic changes with kidney disease in podocytes

被引：71

作者：

Li, Szu Yuan ^{[1
,2
,3
]}

Susztak, Katalin ^{[1
]}

机构：

[1] Univ Penn, Perelman Sch Med, Renal Electrolyte & Hypertens Div, Dept Med, 415 Curie Blvd,405 Clin Res Bldg, Philadelphia, PA 19104 USA

[2] Natl Yang Ming Univ, Div Nephrol, Dept Med, Taipei Vet Gen Hosp, Taipei, Taiwan

[3] Natl Yang Ming Univ, Sch Med, Taipei, Taiwan

来源：

JOURNAL OF CLINICAL INVESTIGATION | 2016年 / 126卷 / 11期

关键词：

MITOCHONDRIAL-FUNCTION; CELLS; MICE;

D O I：

10.1172/JCI90828

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

An increasing amount of evidence suggests that metabolic alterations play a key role in chronic kidney disease (CKD) pathogenesis. In this issue of the JCI, Long et al. report that the long noncoding RNA (lncRNA) taurine-upregulated 1 (Tugi) contributes to CKD development. The authors show that Tugi regulates mitochondria! function in podocytes by epigenetic targeting of expression of the transcription factor PPAR gamma coactivator la (PGC-1 alpha, encoded by Ppargc1a). Transgenic overexpression of Tugi specifically in podocytes ameliorated diabetes induced CKD in mice. Together, these results highlight an important connection between IncRNA-mediated metabolic alterations in podocytes and kidney disease development.

引用

页码：4072 / 4075

页数：4

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