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Quiescent stellate cells represent 5-8% of the total number of liver cells. [4] Each cell has several long cytoplasmic protrusions that extend from the cell body and wrap around the sinusoids. [5] The lipid droplets in the cell body store vitamin A as retinyl palmitate. [6] Hepatic stellate cells store 50–80% of the body's vitamin A. [6]
Cytokines and superoxides go on to cause inflammation and oxidizing damage respectively, while TNFα triggers the stellate cells in the liver to initiate collagen synthesis. These processes result in fibrosis, or scarring of the liver. Fibrosis will eventually cause cirrhosis, a loss of function of the liver due to extensive scarring. [10]
Research has shown the pivotal role of the stellate cell, that normally stores vitamin A, in the development of cirrhosis. Damage to the liver tissue from inflammation leads to the activation of stellate cells, which increases fibrosis through the production of myofibroblasts, and obstructs hepatic blood flow. [60]
Liver cell death and inflammatory responses lead to the activation of hepatic stellate cells, which play a pivotal role in hepatic fibrosis. The extent of fibrosis varies widely. Perisinusoidal fibrosis is most common, especially in adults, and predominates in zone 3 around the terminal hepatic veins. [25]
The Kupffer cells can take up and destroy foreign material such as bacteria. Hepatocytes are separated from the sinusoids by the space of Disse. Hepatic stellate cells are present in the space of Disse and are involved in scar formation in response to liver damage. Defenestration happens when LSECs are lost rendering the sinusoid as an ordinary ...
Liver injury from a number of causes can activate the hepatic stellate cells into transdifferentiated and prolific myofibroblasts. [4] The myofibroblasts synthesize and secrete components of the extracellular matrix including collagen into the perisinusoidal space. [4]
TGF-β1 has been implicated in the process of activating Hepatic Stellate Cells (HSCs) with the magnitude of hepatic fibrosis being in proportion to increase in TGF-β levels. Studies have shown that ACTA2 is associated with TGF-β pathway that enhances contractile properties of HSCs leading to Liver fibrosis. [74]
This is not directly related to the dose of alcohol. Some people seem more prone to this reaction than others. This inflammatory reaction to the fatty change is called alcoholic steatohepatitis and the inflammation probably predisposes to liver fibrosis by activating hepatic stellate cells to produce collagen. [6] Depiction of a liver failure ...