Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8624179 | Experimental and Molecular Pathology | 2018 | 30 Pages |
Abstract
Results herein provide additional evidence that cholestasis induces significant increases in periportal oxidative stress and suggest that there are significant differences in the cellular and subcellular generation of reactive aldehydes formed during cholestatic liver injury. Furthermore, these data suggest that anti-oxidant responses are dysregulated during end-stage PSC/IBD supporting pathological data. This work was funded by NIH5R37AA009300-22 D.R.P.
Keywords
PBSNAFLDMDAWCEαSMACYP2E1CholangiocyteLTXINRSOD2ALTIBDPSCHO-14-HNEGPXGSTPSRAldehyde4-hydroxy-2-nonenalprimary biliary cholangitisMPOROSALDASTAspartate aminotransferaseAlanine aminotransferasealpha smooth muscle actinnonalcoholic steatohepatitisalcoholic liver diseaseNonalcoholic fatty liver diseaseInflammatory bowel diseaseOxidative stressMitochondrial superoxide dismutasecytochrome P4502E1malondialdehydeModel for End-Stage Liver DiseasemyeloperoxidaseInternational Normalized RatioNash heme oxygenase 1Lipid peroxidationLiver transplantPrimary sclerosing cholangitischolestasisMELDglutathione S-transferaseglutathione peroxidaseReactive oxidative species
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Authors
Shearn Colin T., Orlicky David J., Petersen Dennis R.,