The inflammasome in liver injury and non-alcoholic fatty liver disease.

摘要: The liver possesses a strong inflammatory response, as seen experimentally and clinically with inflammation due to toxic metabolic stress, sepsis ischemia. Initiation of this response requires the interaction two types extracellular signals which collectively upregulate activate cytosolic molecular complex termed inflammasome. Signal 1 is via activation pattern recognition receptors, signal 2 delivered by diverse stimuli including particulates adenosine triphosphate. common end result inflammasome protease caspase-1 release active interleukin-1β. important in wide range conditions alcoholic non-alcoholic steatohepatitis. Kupffer cells are known be important, but consequences other hepatic immune have not been well characterized. pathway also required for full fibrotic demonstrated reduced lung, skin fibrosis inflammasome-deficient mice. Identification machinery has opened up novel therapeutic avenues use antagonists Toll-like receptors triphosphate receptor P2X7, interleukin-1 receptor. There now great interest how pathways regulated. initial challenge understand an acute sustained. This significant issue that self-limited under 24 h. suggests there regulators allow sustained such steatohepatitis hepatitis.