Publications by authors named "Xiawen Huang"
In animals, the combination of oxidative liver damage and inhibited hepatocyte proliferation increases the numbers of hepatic progenitors (oval cells). We studied different murine models of fatty liver disease and patients with nonalcoholic fatty liver disease or alcoholic liver disease to determine whether oval cells increase in fatty livers and to clarify the mechanisms for this response. To varying degrees, all mouse models exhibit excessive hepatic mitochondrial production of H(2)O(2), a known inducer of cell-cycle inhibitors.
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- Ethanol sensitizes liver cells (hepatocytes) to the lethal effects of tumor necrosis factor (TNF), but the exact mechanisms are still debated, especially when considering factors present in real-life alcohol-related liver injury.
- A study comparing mice fed ethanol versus a control diet showed that the ethanol-fed mice had a significantly higher liver injury response after exposure to lipopolysaccharide (LPS), despite increased levels of protective cytokines.
- Histological analysis revealed that while control mice showed limited liver damage, ethanol-fed mice exhibited severe damage characterized by ballooned hepatocytes and inflammation, indicating that ethanol alters the liver's response to injury without enhancing apoptotic mechanisms.