Hepatocyte apoptosis and injury

Hepatocyte apoptosis and injury refer to processes by which liver parenchymal cells die or are damaged via intrinsic (mitochondrial/caspase-mediated) or extrinsic (death receptor) pathways. Apoptosis in hepatocytes can be triggered by various insults, including toxins, immune responses, and metabolic disturbances, and contributes to inflammation, fibrosis, and the progression of liver diseases such as NASH and hepatocellular carcinoma. Apoptosis and necrosis are often concentration-dependent and can coexist; excessive apoptosis drives compensatory proliferation and can promote tumorigenesis. Key molecular mediators include the caspase family, BCL-2 family proteins, death receptors (e.g., TRAIL, TNF receptors), mitochondrial permeabilization, and regulatory kinases. Therapeutic inhibitors or modulators of these pathways are under investigation for modifying liver injury outcomes.

Other names

Hepatic apoptosisLiver cell deathHepatocyte injuryHepatic cell damageHepatic necrosis

Caspase inhibition (blocks apoptosis); Necroptosis inhibition (e.g., necrostatin-1); Mitochondrial protection