Figure 3.

Pathogenesis of alcohol-related liver disease and alcohol-induced hepatitis. Excessive alcohol intake cause Kupffer cells and Stellate cells activation along with changes in the microbiome and increased gut permeability. The resulting liver damage, hepatic and systemic inflammation and liver fibrosis are responsible for the dominant clinical consequences seen in AH patients. In addition, expansion of immature progenitor cells leads to impaired regeneration and HNF4a P2 variants are seen expressed in AH. LPS, lipopolysaccharide; NADPH, nicotinamide adenine dinucleotide phosphate; NFκB, nuclear factor kappa B; TNF, tumoral necrosis factor; ROS, reactive oxygen species; HSC, hepatic stellate cell; TGF-β, transforming growth factor-β; STAT, signal transducers and activators of transcription; SIRS, systemic inflammatory response syndrome; HNF4A, hepatocyte nuclear factor 4 alpha; AH, alcohol-induced hepatitis.