6533b873fe1ef96bd12d4c68
RESEARCH PRODUCT
Inflammasomes in Liver Fibrosis
Pablo PelegrínFernando AlegreFernando AlegreAriel E. Feldsteinsubject
Liver Cirrhosis0301 basic medicinemedicine.medical_treatmentAnti-Inflammatory AgentsCaspase 1BiologyLiver transplantationProinflammatory cytokine03 medical and health sciencesLiver diseaseFibrosisNLR Family Pyrin Domain-Containing 3 ProteinPyroptosismedicineAlarminsAnimalsHumansHepatologyPyroptosisInflammasomemedicine.disease030104 developmental biologyReceptors Pattern RecognitionImmunologyHepatic stellate cellInflammation MediatorsSignal Transductionmedicine.drugdescription
AbstractCell death and inflammation are two central elements in the development of liver fibrosis. Inflammasomes are intracellular multiprotein complexes expressed in both hepatocytes and nonparenchymal cells in the liver that are key regulators of inflammation and cell fate. They respond to cellular danger signals by activating caspase 1, releasing the proinflammatory cytokines IL-1β and IL-18, as well as initiating a novel pathway of programmed cell death termed “pyroptosis.” These processes can initiate and perpetuate an abnormal wound-healing response with the principle cellular target being the activation of hepatic stellate cells. From the various inflammasomes, the NLRP3 inflammasome has been increasingly implicated in the pathogenesis of chronic inflammatory liver diseases, including nonalcoholic steatohepatitis, a disease process that is soaring and has evolved as a primary cause of liver fibrosis and need for liver transplantation. In this review, the authors highlight the growing evidence for both indirect and direct effects of inflammasomes in triggering liver fibrosis as well as potential novel targets for antifibrotic therapies.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2017-05-01 | Seminars in Liver Disease |