The long noncoding RNA Tug1 connects metabolic changes with kidney disease in podocytes
Szu Yuan Li, Katalin Susztak
Szu Yuan Li, Katalin Susztak
Published October 17, 2016
Citation Information: J Clin Invest. 2016;126(11):4072-4075. https://doi.org/10.1172/JCI90828.
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Commentary

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

Abstract

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 (Tug1) contributes to CKD development. The authors show that Tug1 regulates mitochondrial function in podocytes by epigenetic targeting of expression of the transcription factor PPARγ coactivator 1α (PGC-1α, encoded by Ppargc1a). Transgenic overexpression of Tug1 specifically in podocytes ameliorated diabetes-induced CKD in mice. Together, these results highlight an important connection between lncRNA-mediated metabolic alterations in podocytes and kidney disease development.

Authors

Szu Yuan Li, Katalin Susztak

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Figure 2

Proper mitochondrial function is essential for podocyte health in diabetes.

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Proper mitochondrial function is essential for podocyte health in diabet...
Tug1 expression is decreased in diabetic podocytes. Tug1 regulates PGC-1α expression by epigenetic targeting. Decreased PGC-1α levels results in structural and functional mitochondrial changes. Impaired mitochondrial function will cause energy depletion, increased ROS generation, and, ultimately, the development of diabetic kidney disease. DKD, diabetic kidney disease; NOX4, NAPDH oxidase 4.