The long noncoding RNA Tug1 connects metabolic changes with kidney disease in podocytes.
basic_science · Level V
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- Record sourced from PubMed, PMID 27760046.
- Also identified by DOI 10.1172/JCI90828 and PMC identifier 5096895.
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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.
Medical subject headings
- Diabetic Nephropathies
- Epigenesis, Genetic
- Mitochondria
- Podocytes
- RNA, Long Noncoding
- Renal Insufficiency, Chronic