6533b82dfe1ef96bd1291425

RESEARCH PRODUCT

Apoptosis in liver disease

Marcus SchuchmannPeter R. Galle

subject

ProteasesProgrammed cell deathApoptosisLigandsReceptors Tumor Necrosis FactorFas ligandTransforming Growth Factor beta1Antigens CDTransforming Growth Factor betaExtracellularAnimalsHumansfas ReceptorCaspaseHepatologybiologyLiver DiseasesGastroenterologyFas receptorCell biologyBiochemistryReceptors Tumor Necrosis Factor Type IApoptosisCaspasesbiology.proteinIntracellular

description

A variety of biological functions are regulated through extracellular signals. Amongst the best studied examples is growth control, which is achieved by the regulatory function of growth factors. In recent years it has become apparent that cell death (apoptosis) is controlled in a similar fashion. Apoptosis, firstly a morphologically defined process, is a highly controlled type of cell death that plays a critical role in embryonic development, deletion of autoreactive T-cells and adult tissue homoeostasis. There is increasing evidence that derangement of the apoptotic program is the underlying cause of a series of diseases including liver diseases. The deadly program can be initiated by ligand binding to membrane bound receptors such as CD95 (Fas), which is the most prominent cell death inducing member of the TNF receptor superfamily. The core of the subsequently activated intracellular machinery is formed by a set of proteases, namely caspases. Once activated, they orchestrate the complete destruction of the cellular skeleton leading to the typical apoptotic morphology. This review foucuses on the underlying mechanism leading to derangement of the usually highly controlled apoptotic program in different liver diseases.

https://doi.org/10.1097/00042737-200107000-00005