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Genetic Nrf2 Overactivation Inhibits the Deleterious Effects Induced by Hepatocyte-Specific c-met Deletion during the Progression of NASH. | LitMetric

AI Article Synopsis

  • Recent findings indicate that liver cells lacking the c-met receptor speed up the progression of nonalcoholic steatohepatitis by increasing harmful reactive oxygen species and fibrosis development.
  • This study investigates how overactivation of the Nrf2 protein affects liver cells without c-met, leading to a significant imbalance between harmful and protective oxidative responses.
  • Results show that genetically activating Nrf2 in double knockout mice improved liver health by reducing oxidative stress and fibrosis, suggesting potential therapeutic avenues for liver diseases.

Article Abstract

We have recently shown that hepatocyte-specific c-met deficiency accelerates the progression of nonalcoholic steatohepatitis in experimental murine models resulting in augmented production of reactive oxygen species and accelerated development of fibrosis. The aim of this study focuses on the elucidation of the underlying cellular mechanisms driven by Nrf2 overactivation in hepatocytes lacking c-met receptor characterized by a severe unbalance between pro-oxidant and antioxidant functions. Control mice (c-met), single c-met knockouts (c-met), and double c-met/Keap1 knockouts (met/Keap1) were then fed a chow or a methionine-choline-deficient (MCD) diet, respectively, for 4 weeks to reproduce the features of nonalcoholic steatohepatitis. Upon MCD feeding, met/Keap1 mice displayed increased liver mass albeit decreased triglyceride accumulation. The marked increase of oxidative stress observed in c-met was restored in the double mutants as assessed by 4-HNE immunostaining and by the expression of genes responsible for the generation of free radicals. Moreover, double knockout mice presented a reduced amount of liver-infiltrating cells and the exacerbation of fibrosis progression observed in c-met livers was significantly inhibited in met/Keap1. Therefore, genetic activation of the antioxidant transcription factor Nrf2 improves liver damage and repair in hepatocyte-specific c-met-deficient mice mainly through restoring a balance in the cellular redox homeostasis.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5476895PMC
http://dx.doi.org/10.1155/2017/3420286DOI Listing

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