期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 126, 期 11, 页码 4072-4075出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI90828
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资金
- NIDDK NIH HHS [R01 DK087635, DP3 DK108220, R01 DK076077] Funding Source: Medline
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.
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