Why the study?
Non-alcoholic steatohepatitis has increasingly become a major cause of liver cirrhosis and liver cancer, with emerging findings highlighting functional sex-based differences, cell stress, and cell death.
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Design
Review
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This review highlights the role of B cell lymphoma 6 in regulating sex-based differences in NASH-induced liver injury and tumorigenesis.
The liver is a crucial organ for maintaining homeostasis in living organisms and is the center of various metabolic functions. Therefore, abnormal metabolic activity, as in metabolic syndrome, leads to pathological conditions, such as abnormal accumulation of lipids in the liver. Inflammation and cell death are induced by several stresses in the fatty liver, namely steatohepatitis. In recent years, an increase in non-alcoholic steatohepatitis (NASH), which is not dependent on excessive alcohol intake, has become an issue as a major cause of liver cirrhosis and liver cancer. There are several recent findings on functional sex-based differences, NASH, and cell stress and death in the liver. In particular, NASH-induced liver injury and tumorigeneses were suppressed by B cell lymphoma 6, the transcriptional factor regulating sex-based liver functional gene expression. In this review, we discuss cell response to stress and lipotoxicity in NASH and its regulatory mechanisms.
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Kamiya et al. (2022) studied this question.
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