Inflammation in Alcoholic Liver Disease
Year: 2012
Type: review
Abstract: Frank Burr Mallory's landmark observation in 1911 on the histopathology of alcoholic liver disease (ALD) was the first identification of a link between inflammation and ALD. In this review, we summarize recent advances regarding the origins and roles of various inflammatory components in ALD. Metabolism of ethanol generates a number of metabolites, including acetate, reactive oxygen species, acetaldehyde, and epigenetic changes, that can induce inflammatory responses. Alcohol and its metabolites can also initiate and aggravate inflammatory conditions by promoting gut leakiness of microbial products, by sensitizing immune cells to stimulation, and by activating innate immune pathways, such as complement. Chronic alcohol consumption also sensitizes nonimmune cells, e.g., hepatocytes, to inflammatory signals and impairs their ability to respond to protective signals. Based on these advances, a number of inflammatory targets have been identified with potential for therapeutic intervention in ALD, presenting new opportunities and challenges for translational research.
Source: Annual Review of Nutrition
Authors: H. Joe Wang, Bin Gao, Samir Zakhari, Laura E. Nagy
Language: English
Subfield: Pathology and Forensic Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: green
Awards: G1997962874, Molecular mechanisms of liver injury, repair, and immunity, Insulin Mediated Glucose Transport Disrupt by Ethanol., Ethanol regulation of Kupffer cell signal transduction, Alcoholic liver disease: Biochemical, cellular and systemic responses to ethanol, Role of Adipose in Ethanol-Induced Tissue Injury, Complement and ethanol-induced liver injury., Pathogenesis and Novel Therapeutic Targets of Steatotic Liver Disease and Cancer
OpenAlex ID: W2114405620
