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.
Publication types
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Research Support, N.I.H., Extramural
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Comment
MeSH terms
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Animals
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Diabetic Nephropathies* / genetics
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Diabetic Nephropathies* / metabolism
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Diabetic Nephropathies* / pathology
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Epigenesis, Genetic*
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Mice
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Mitochondria* / genetics
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Mitochondria* / metabolism
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Mitochondria* / pathology
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Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha / biosynthesis
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Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha / genetics
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Podocytes* / metabolism
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Podocytes* / pathology
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RNA, Long Noncoding* / genetics
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RNA, Long Noncoding* / metabolism
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Renal Insufficiency, Chronic* / genetics
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Renal Insufficiency, Chronic* / metabolism
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Renal Insufficiency, Chronic* / pathology
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Transgenes
Substances
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Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
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Ppargc1a protein, mouse
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RNA, Long Noncoding
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long non-coding RNA TUG1, mouse