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Defective fatty acid oxidation in renal tubular epithelial cells has a key role in kidney fibrosis development
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Defective fatty acid oxidation in renal tubular epithelial cells has a key role in kidney fibrosis development
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Journal Article
Defective fatty acid oxidation in renal tubular epithelial cells has a key role in kidney fibrosis development
2015
Overview
A new study shows that reduced fat metabolism in renal tubule cells contributes to kidney fibrosis.
Renal fibrosis is the histological manifestation of a progressive, usually irreversible process causing chronic and end-stage kidney disease. We performed genome-wide transcriptome studies of a large cohort (
n
= 95) of normal and fibrotic human kidney tubule samples followed by systems and network analyses and identified inflammation and metabolism as the top dysregulated pathways in the diseased kidneys. In particular, we found that humans and mouse models with tubulointerstitial fibrosis had lower expression of key enzymes and regulators of fatty acid oxidation (FAO) and higher intracellular lipid deposition compared to controls.
In vitro
experiments indicated that inhibition of FAO in tubule epithelial cells caused ATP depletion, cell death, dedifferentiation and intracellular lipid deposition, phenotypes observed in fibrosis. In contrast, restoring fatty acid metabolism by genetic or pharmacological methods protected mice from tubulointerstitial fibrosis. Our results raise the possibility that correcting the metabolic defect in FAO may be useful for preventing and treating chronic kidney disease.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject
