Journal
CELLS
Volume 9, Issue 2, Pages -Publisher
MDPI
DOI: 10.3390/cells9020461
Keywords
liver inflammation; liver fibrosis; sterile inflammation; inflammasome; DAMPs
Categories
Funding
- Romanian Ministry of Research and Innovation, CCDI-UEFISCDI within PNCDI III [PN-III-P1-1.2-PCCDI-2017-0407/INTELMAT, PN-III-P1-1.2-PCCDI-2017-0341/PATHDERM, PN-III-P1-1.2-PCCDI-2017-0782/REGMED]
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Inflammation has been known to be an important driver of fibrogenesis in the liver and onset of hepatic fibrosis. It starts off as a process meant to protect the liver from further damage, but it can become the main promoter of liver fibrosis. There are many inflammation-related pathways activated during liver fibrosis that lead to hepatic stellate cells (HSCs) activation and collagen-deposition in the liver. Such events are mostly modulated upstream of HSCs and involve signals from hepatocytes and innate immune cells. One particular event is represented by cell death during liver injury that generates multiple inflammatory signals that further trigger sterile inflammation and enhancement of inflammatory response. The assembly of inflammasome that responds to danger-associated molecular patterns (DAMPs) stimulates the release of pro-inflammatory cytokines and at the same time, initiates programmed cell death called pyroptosis. This review focuses on cellular and molecular mechanisms responsible for initiation and progress of inflammation in the liver.
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