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Cellular Interplay as a Consequence of Inflammatory Signals Leading to Liver Fibrosis Development.


ABSTRACT: 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.

SUBMITTER: Ignat SR 

PROVIDER: S-EPMC7072785 | biostudies-literature | 2020 Feb

REPOSITORIES: biostudies-literature

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Cellular Interplay as a Consequence of Inflammatory Signals Leading to Liver Fibrosis Development.

Ignat Simona-Rebeca SR   Dinescu Sorina S   Hermenean Anca A   Costache Marieta M  

Cells 20200218 2


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  ...[more]

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