Defective fatty acid oxidation in renal tubular epithelial cells has a key role in kidney fibrosis development View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2015-01

AUTHORS

Hyun Mi Kang, Seon Ho Ahn, Peter Choi, Yi-An Ko, Seung Hyeok Han, Frank Chinga, Ae Seo Deok Park, Jianling Tao, Kumar Sharma, James Pullman, Erwin P Bottinger, Ira J Goldberg, Katalin Susztak

ABSTRACT

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. More... »

PAGES

37-46

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nm.3762

DOI

http://dx.doi.org/10.1038/nm.3762

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1045967711

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/25419705


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