| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 8632903 | Metabolism | 2018 | 36 Pages |
Abstract
These findings identified a negative feedback loop between miR-378 and Nrf1 that promotes the pathogenesis of hepatosteatosis, and suggests the use of miR-378 as a potential therapeutic target for NAFLD.
Keywords
acyl-coenzyme A oxidase 1acyl-CoA dehydrogenase, very long chain3′UTRsNAFLDVLCADGPATAnti-sense oligonucleotidestearoyl-CoA desaturase-1SCD1OCRSREBPsNRF1PPARαACOX1Cpt1aHFDASOORFFFA3′ untranslated regionsH&EHCCperoxisome proliferator-activated receptor alphanonalcoholic steatohepatitisFree fatty acidfatty acid synthaseFatty acid oxidationchromatin immunoprecipitationnon-alcoholic fatty liver diseasehematoxylin and eosin stainHigh fat dietFAOFasnopen reading frameTranscription regulationOxygen consumption rateMicroRNANash Hepatosteatosissterol regulatory element-binding proteinsCHiPHepatocellular carcinomacarnitine palmitoyltransferase 1aglycerol-3-phosphate acyltransferase
Related Topics
Life Sciences
Biochemistry, Genetics and Molecular Biology
Endocrinology
Authors
Tianpeng Zhang, Xiaoling Zhao, Clifford J. Steer, Guiqin Yan, Guisheng Song,