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Our study demonstrated that inactivation of RIPK1 kinase through the introduction of the Ripk1 D138N mutation in hepatocellular HK2-deficient mice significantly ameliorated liver pathology by preventing hepatocyte apoptosis and subsequently reducing the development of HCC

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While these models present additional challenges, they can provide valuable insights into the complex interactions between TBI and other factors, leading to improved understanding of the disease and the development of more effective treatments

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[DOI] [PMC free article] [PubMed] [Google Scholar] 87.Jiang A.Y., Witten J., Raji I.O., Eweje F., MacIsaac C., Meng S., et al
