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The prevailing theory for the development of autoimmune hepatitis is thought to be the interplay of genetic predisposition, an environmental trigger (virus, drugs, herbs, immunizations), and failure of the native immune system resulting in chronic inflammation of hepatocytes and subsequent fibrosis of the liver. [7] [8] [9]
This results in tissue damage to the endothelium because of proteases, oxygen radicals, prostanoids and other substances from leukocytes. Kupffer cell activation contributes to pathogenesis of both chronic and acute alcoholic liver disease in response to ethanol-induced liver injury, common in chronic alcoholics. Chronic alcoholism and liver ...
This manifests as lipid peroxidation, mitochondrial damage, and glutathione (an endogenous antioxidant) depletion. [7] Damaged hepatocytes release Danger associated molecular patterns (DAMPs) which are molecules that lead to further activation of the immune system's inflammatory response and further hepatocyte damage. [7]
Cirrhosis associated immune dysfunction is caused by reduced complement component synthesis in the liver including C3, C4 and reduced total complement activity . [130] The complement system is a part of the innate immune system and assists immune cells and antibodies in destroying pathogens. The liver produces compliment factors, but this may ...
Liver regeneration is the process by which the liver is able to replace damaged or lost liver tissue. The liver is the only visceral organ with the capacity to regenerate. [1] [2] The liver can regenerate after partial hepatectomy or injury due to hepatotoxic agents such as certain medications, toxins, or chemicals. [3]
In vitro model systems based on hepatocytes have been of great help to better understand the role of hepatocytes in (patho)physiological processes of the liver. In addition, pharmaceutical industry has heavily relied on the use of hepatocytes in suspension or culture to explore mechanisms of drug metabolism and even predict in vivo drug metabolism.
The increase in intracellular reactive oxygen species is about 10,000-fold with chronic hepatitis B virus infection and 100,000-fold following hepatitis C virus infection. [25] This increase in reactive oxygen species causes inflammation [25] and more than 20 types of DNA damage. [26]
Physical agents such as heat or radiation can damage a cell by literally cooking or coagulating their contents. Impaired nutrient supply, such as lack of oxygen or glucose, or impaired production of adenosine triphosphate (ATP) may deprive the cell of essential materials needed to survive. [3] Metabolic: Hypoxia and ischemia; Chemical agents