Hepatic Stellate Cells as a Target for the Treatment of Liver Fibrosis
Pragati Lingwal, Ganesh Kumar Bhatt, Preeti Kothiyal, Shri Guru, R. C.
Abstract
Pragati Lingwal, Ganesh Kumar Bhatt, Preeti Kothiyal, Shri Guru, R. C.
Abstract
Liver fibrosis as the final common end stage of most chronic liver diseases is triggered by chronic liver injury caused by various etiologies including viral infection, cholestasis, metabolic diseases and alcohol abuse. It is reversible wound-healing response characterized by the accumulation of extracellular matrix proteins (ECM) including collagen. Hepatic stellate cells (HSCs) are the major source of extracellular matrix components and are the key mediators of fibrogenesis. Hepatic stellate cells are definitely involved in the pathogenesis of various liver pathologies, besides the well know key role in fibrosis and extracellular matrix remodelling. Potent drugs may not be effective enough in the treatment of liver fibrosis. The inflammatory cytokines produced by kupffer cells, the liver resident macrophage, aggravate liver fibrosis. Transforming growth factor β1 (TGF- β1) is also activator of HSCs. Liver fibrosis is a serious healthcare problem with high morbidity and motility. It is the result of wound healing responses to repeated liver injury irrespective of etiology. With the development of the diseases, excessive extracellular matrix (ECM) components are deposited in the liver, leading to portal hypertension, cirrhosis or hepatocellular carcinoma .Normally HSCs are quiescent in nature but when liver have any injury they get activated and releases extracellular matrix proteins. The review describes the use of HSCs, transforming growth factor β1 for therapeutic purposes in liver fibrosis.
OpenAlex reports 6 citations for this work. Citation counts describe recorded attention and do not establish research quality.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
Liver fibrosis as the final common end stage of most chronic liver diseases is triggered by chronic liver injury caused by various etiologies including viral infection, cholestasis, metabolic diseases and alcohol abuse. It is reversible wound-healing response characterized by the accumulation of extracellular matrix proteins (ECM) including collagen. Hepatic stellate cells (HSCs) are the major source of extracellular matrix components and are the key mediators of fibrogenesis. Hepatic stellate cells are definitely involved in the pathogenesis of various liver pathologies, besides the well know key role in fibrosis and extracellular matrix remodelling. Potent drugs may not be effective enough in the treatment of liver fibrosis. The inflammatory cytokines produced by kupffer cells, the liver resident macrophage, aggravate liver fibrosis. Transforming growth factor β1 (TGF- β1) is also activator of HSCs. Liver fibrosis is a serious healthcare problem with high morbidity and motility. It is the result of wound healing responses to repeated liver injury irrespective of etiology. With the development of the diseases, excessive extracellular matrix (ECM) components are deposited in the liver, leading to portal hypertension, cirrhosis or hepatocellular carcinoma .Normally HSCs are quiescent in nature but when liver have any injury they get activated and releases extracellular matrix proteins. The review describes the use of HSCs, transforming growth factor β1 for therapeutic purposes in liver fibrosis.
Key concepts: Hepatic stellate cell, Extracellular matrix, Fibrosis, Cirrhosis, Chronic liver disease, Medicine, Liver injury, Hepatic fibrosis