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- W4211018071 abstract "Death of constituent cell populations of the liver is a central component of liver injury cascades. Cell death in the liver can occur via regulated (apoptosis or necroptosis) or unregulated (necrosis) mechanisms. Apoptosis can be initiated via death receptor-mediated pathways known as the extrinsic pathway or from intracellular perturbations known as the intrinsic pathway. Mitochondrial permeabilization is required for efficient hepatocyte apoptosis, and both intrinsic and extrinsic pathways converge on mitochondria. Effector caspases are activated downstream of mitochondria, and cleave several cellular targets to result in the characteristic apoptotic morphology. Necroptosis is initiated by death receptors when caspases are inhibited. It is mediated by receptor interacting kinase 1 and 3 which culminate in activation of mixed lineage kinase domain-like protein, a pseudokinase which forms pores in the plasma membrane leading to death receptor-activated caspase-independent cell death termed necroptosis. Unregulated cell death causes necrosis by accidental mechanisms causing cell swelling and plasma membrane rupture. Injured and dying cells release extracellular vesicles and damage-associated molecular patterns that activate the innate immune system and downstream inflammatory cascades. Ongoing cell death in the liver recruits proinflammatory myeloid cells and activates tissue macrophages and fibrogenic hepatic stellate cells. Inflammation and fibrosis promoting crosstalk between diseased hepatocytes and other constituent liver cells often promotes liver injury by feed-forward processes. Therapies aimed at preventing hepatocyte cell death show promise in experimental and clinical settings." @default.
- W4211018071 created "2022-02-13" @default.
- W4211018071 creator A5002077162 @default.
- W4211018071 creator A5004470985 @default.
- W4211018071 date "2017-10-23" @default.
- W4211018071 modified "2023-10-14" @default.
- W4211018071 title "Mechanisms of Liver Injury" @default.
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