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

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.