• RIPK1
• MLKL
• apoptosis
• necroptosis
• TNF
• BDL
• Fragile X mental retardation

Acute and chronic liver diseases due to various pathogens have in common that cellular stress and cell death represent their initial triggers. While in acute liver damage and especially in acute liver failure, the loss of functional hepatocytes is the dominant, life-limiting factor, low levels of cell death in chronic diseases like non-alcoholic fatty liver (NASH) or alcoholic liver disease initiate a cascade of immunological cell death responses, driving the progression to liver cirrhosis and finally to hepatocellular carcinoma.1 On a molecular level, hepatocytes that undergo programmed cell death release factors known as danger-associated molecular patterns, which activate immune cells (macrophages) and hepatic stellate cells, and are thus involved in chronic phase transition of liver diseases and decompensation.1

For years, the term apoptosis was used synonymously with the term ‘programmed cell death’. Nevertheless, this highly simplified dogma was swept away over night when it was discovered that apoptosis was accompanied by several other programmed cell death signalling pathways, and that necrosis was not only a passive form of cell death, for example, in the context of ischaemia, but that …