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Liver fibrosis is a major cause of morbidity and mortality worldwide as a result of chronic liver injury. Liver fibrosis is a scarring process, eventually leading to liver cirrhosis and cancer, and represents the final common pathway for most chronic liver diseases including viral hepatitis, alcoholic hepatitis and, more recently, fatty liver disease associated with obesity.1 Fibrosis is characterised by both quantitative and qualitative changes in the composition of the connective tissue, which results from the imbalance between the production and degradation of extracellular matrix components. Fibrosis is part of the liver's wound-healing response and is preceded by an inflammatory response, which is the driving force for the progressive accumulation of extracellular matrix components in the liver.1
Hepatic stellate cells (HSC) play a pivotal role in the initiation and progression of hepatic fibrosis.2 HSC are resident vitamin A-storing cells located in the space of Disse between the fenestrated sinusoidal endothelium and the layer of hepatocytes. Scattered within the sinusoidal lining and in direct contact with the blood are the Kupffer cells, the professional resident macrophages involved in detoxification processes. This complex architecture of the hepatic sinusoid ensures full hepatic functionality by providing a unique environment where each single hepatocyte is in close contact with these sinusoidal cells as well as with other hepatocytes. The paradigm in liver injury is initiated when Kupffer cells are activated by lipid peroxidation products derived from damaged hepatocytes or in response to increased …
Linked article 301400.
Funding JC is supported by a grant from the Ministerio de Ciencia e Innovación (MICINN) (SAF 09/08767).
Competing interests None.
Provenance and peer review Commissioned; externally peer reviewed.
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