2024
DOI: 10.1016/j.xcrm.2024.101401
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p63 controls metabolic activation of hepatic stellate cells and fibrosis via an HER2-ACC1 pathway

Marcos F. Fondevila,
Eva Novoa,
Maria J. Gonzalez-Rellan
et al.
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Cited by 2 publications
(1 citation statement)
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“…Another study showed that G proteincoupled receptor (GPCR) activation mediated PKM2 upregulation, which in turn enhanced glycolysis in Kupffer cells and suppressed hepatic inflammation, thereby alleviating highfat diet-induced obesity and MAFLD [109]. The activation of hepatic stellate cells (HSCs) is considered to be a key mechanism leading to liver fibrosis in MAFLD, and enhanced glycolysis contributes to HSCs activation and promotes the expression of fibrosis-related genes [110][111][112][113]. More importantly, over-enhanced glycolysis in hepatocytes predicts the tendency toward hepatocellular carcinoma, as tumor cells prefer to break down glucose into lactate via glycolysis to meet the energy demands for rapid proliferation, namely, the Warburg effect [114].…”
Section: Glycolysis and Mafldmentioning
confidence: 99%
“…Another study showed that G proteincoupled receptor (GPCR) activation mediated PKM2 upregulation, which in turn enhanced glycolysis in Kupffer cells and suppressed hepatic inflammation, thereby alleviating highfat diet-induced obesity and MAFLD [109]. The activation of hepatic stellate cells (HSCs) is considered to be a key mechanism leading to liver fibrosis in MAFLD, and enhanced glycolysis contributes to HSCs activation and promotes the expression of fibrosis-related genes [110][111][112][113]. More importantly, over-enhanced glycolysis in hepatocytes predicts the tendency toward hepatocellular carcinoma, as tumor cells prefer to break down glucose into lactate via glycolysis to meet the energy demands for rapid proliferation, namely, the Warburg effect [114].…”
Section: Glycolysis and Mafldmentioning
confidence: 99%