Metabolic inflammation as an instigator of fibrosis during non-alcoholic fatty liver disease.

Abstract:

:Non-alcoholic fatty liver disease (NAFLD) is characterized by excessive storage of fatty acids in the form of triglycerides in hepatocytes. It is most prevalent in western countries and includes a wide range of clinical and histopathological findings, namely from simple steatosis to steatohepatitis and fibrosis, which may lead to cirrhosis and hepatocellular cancer. The key event for the transition from steatosis to fibrosis is the activation of quiescent hepatic stellate cells (qHSC) and their differentiation to myofibroblasts. Pattern recognition receptors (PRRs), expressed by a plethora of immune cells, serve as essential components of the innate immune system whose function is to stimulate phagocytosis and mediate inflammation upon binding to them of various molecules released from damaged, apoptotic and necrotic cells. The activation of PRRs on hepatocytes, Kupffer cells, the resident macrophages of the liver, and other immune cells results in the production of proinflammatory cytokines and chemokines, as well as profibrotic factors in the liver microenvironment leading to qHSC activation and subsequent fibrogenesis. Thus, elucidation of the inflammatory pathways associated with the pathogenesis and progression of NAFLD may lead to a better understanding of its pathophysiology and new therapeutic approaches.

journal_name

World J Gastroenterol

authors

Katsarou A,Moustakas II,Pyrina I,Lembessis P,Koutsilieris M,Chatzigeorgiou A

doi

10.3748/wjg.v26.i17.1993

subject

Has Abstract

pub_date

2020-05-07 00:00:00

pages

1993-2011

issue

17

eissn

1007-9327

issn

2219-2840

journal_volume

26

pub_type

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