Lipotoxicity pathways intersect in hepatocytes: Endoplasmic reticulum stress, c-Jun N-terminal kinase-1, and death receptors.
作者： Yuko Akazawa , Kazuhiko Nakao
DOI: 10.1111/HEPR.12658
关键词:
摘要: Non-alcoholic fatty liver disease (NAFLD) is becoming increasingly more common worldwide. Hepatocyte apoptosis caused by free acids, termed hepatocyte lipoapoptosis, a feature of non-alcoholic steatohepatitis (NASH), an advanced form NAFLD. As no salutary treatment for NASH exists, it important to understand the molecular mechanisms responsible development and progression. This review discusses recent developments in research on focusing endoplasmic reticulum stress, c-Jun N-terminal kinase-1, death receptor-mediated pathway networks their modulators interactions. In addition, we describe emerging importance signaling pathways that not only impact dying hepatocytes themselves, but also influence surrounding cells possibly promote progression through release microvesicles. Overall, comprehensive understanding mediators lipotoxicity-related would likely benefit mechanism-based therapies NASH.
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