High-Mobility Group Box-1 (HMGB1) participates in the pathogenesis of alcoholic liver disease (ALD)

The HMGB1/RAGE axis triggers neutrophil-mediated injury amplification following necrosis

“…In light of recent reports indicating that posttranslational modifications of HMGB1 modulate its bioactivity, we used proteomic mass spectrometry (MS) and tandem mass spectrometry (MS/MS) (39) to identify the presence of HMGB1 posttranslational modifications in the serum of acetaminophen-treated mice and to assign them to specific cellular sources. We observed the presence of 4 distinct and amplifies injury in vivo, focusing on Toll-like receptor 4 (TLR4) and the receptor for advanced glycation end-products (RAGE) as the best-established HMGB1 receptors (41).…”

RGC-32 Deficiency Protects against Hepatic Steatosis by Reducing Lipogenesis

“…Alcoholic fatty liver is the earliest and most common response of the liver to alcohol and may be a precursor of more severe forms of liver injury, like steatohepatitis, progressive fibrosis, cirrhosis, and hepatocellular carcinoma (4,49). Although the pathogenesis and diagnosis are different between nonalcoholic and alcoholic fatty liver disease, excessive triglyceride accumulation in the liver induced by activation of lipogenesis is their common feature.…”

Effect of SIRS and sepsis on mortality in alcoholic hepatitis: A systematic review and meta-analysis

“…In mouse models for alcoholic hepatitis, the inhibition of DAMPs was shown to decrease proinflammatory cytokines, the degree of liver inflammation, and liver steatosis (29,30). The identification of DAMPs and further determination of the effect of pharmacologic DAMPs inhibition might guide future immunotherapeutic intervention in order to limit the inflammatory response and to potentially improve the outcome.…”