PMID: 19928668Nov 26, 2009Paper

The bile acids as an example of patogens destructive hepatocytes in alcoholic liver injury

Polski merkuriusz lekarski : organ Polskiego Towarzystwa Lekarskiego
Ewa OgłodekDanuta Moś

Abstract

Chronic cholestasis in alcoholic liver disease contributes to the death of hepatocyte by either apoptotic or necrotic pathways. The hydrophobic acid inducing toxins in hepatocytes and cholangiocytes cause the perturbation of their mitochondrial membrane, marginal condensation of chromatin and also proteolytic digestion of the cell structure. In the activation of the apoptosis mechanism in hepatocytes the following cytokines take part: the Fas system, TNF alpha. The proteins Bcl-x(L) and Bcl-w inhibit apoptosis, while Bax and Bad protein promotes it. The Bax protein interacts with mitochondrial pores inducing cytochrome c, which contributes to the release of caspase-activated proteins and starts the apoptosis. The development of the new therapeutic strategies by protecting hepatocytes from apoptosis remains very important research for the nearest future.

Related Concepts

Related Feeds

BCL-2 Family Proteins

BLC-2 family proteins are a group that share the same homologous BH domain. They play many different roles including pro-survival signals, mitochondria-mediated apoptosis and removal or damaged cells. They are often regulated by phosphorylation, affecting their catalytic activity. Here is the latest research on BCL-2 family proteins.

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis

Apoptotic Caspases

Apoptotic caspases belong to the protease enzyme family and are known to play an essential role in inflammation and programmed cell death. Here is the latest research.