Rethinking carnitine palmitoyltransferase II and liver stem cells in metabolic dysfunction-associated fatty liver disease-related hepatocellular carcinoma DOI
Hong Cai, Chunhui Yang, Peng Gao

et al.

World Journal of Gastroenterology, Journal Year: 2025, Volume and Issue: 31(15)

Published: April 17, 2025

This article discusses a recent study by Wang et al that sheds light on the metabolic and immunological mechanisms driving progression of dysfunction-associated fatty liver disease (MAFLD) to hepatocellular carcinoma (HCC). The highlights role mitochondrial carnitine palmitoyltransferase II (CPT II) inactivity, which activates cancer stem cells marked cluster differentiation 44 (CD44) CD24 expression, promoting HCC development. Using dynamic mouse models clinical samples, identified CPT downregulation, membrane potential alterations, reduced intrahepatic CD4+ T cell as key drivers progression. findings link these changes steroid biosynthesis p53 signaling, contributing T-cell dysfunction immunosuppression. emphasizes relevance results in understanding MAFLD pathogenesis therapeutic strategies targeting activity, function, immune surveillance prevent or mitigate development advanced MAFLD.

Language: Английский

Rethinking carnitine palmitoyltransferase II and liver stem cells in metabolic dysfunction-associated fatty liver disease-related hepatocellular carcinoma DOI
Hong Cai, Chunhui Yang, Peng Gao

et al.

World Journal of Gastroenterology, Journal Year: 2025, Volume and Issue: 31(15)

Published: April 17, 2025

This article discusses a recent study by Wang et al that sheds light on the metabolic and immunological mechanisms driving progression of dysfunction-associated fatty liver disease (MAFLD) to hepatocellular carcinoma (HCC). The highlights role mitochondrial carnitine palmitoyltransferase II (CPT II) inactivity, which activates cancer stem cells marked cluster differentiation 44 (CD44) CD24 expression, promoting HCC development. Using dynamic mouse models clinical samples, identified CPT downregulation, membrane potential alterations, reduced intrahepatic CD4+ T cell as key drivers progression. findings link these changes steroid biosynthesis p53 signaling, contributing T-cell dysfunction immunosuppression. emphasizes relevance results in understanding MAFLD pathogenesis therapeutic strategies targeting activity, function, immune surveillance prevent or mitigate development advanced MAFLD.

Language: Английский

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