CD95/CD95L-mediated apoptosis of the hepatic stellate cell. A mechanism terminating uncontrolled hepatic stellate cell proliferation during hepatic tissue repair.
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Summary
It is demonstrated that apoptotic HSC were detectable in parallel with HSC activation, which suggests that apoptosis might represent an important mechanism terminating proliferation of activated HSC.
- Type
- article
- Published
- 1997-11-01
- Cited by
- 182
- References
- 42
- Access
- Open access
- OpenAlex
- https://openalex.org/W66029348
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:37122530
Keywords
Hepatic stellate cell, Apoptosis, Cell biology, Biology, Fas receptor
References
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- Different populations of macrophages use either the vitronectin receptor or the phosphatidylserine receptor to recognize and remove apoptotic cells.
- The heterogeneity of mononuclear phagocytes in lymphoid organs: distinct macrophage subpopulations in rat recognized by monoclonal antibodies ED1, ED2 and ED3.
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- Fat storing cells (FSC) of rat liver synthesize and secrete fibronectin. Comparison with hepatocytes.
- The Bcl-2 oncoprotein functions as a pro-oxidant.
- Hemorrhage in lesions caused by cowpox virus is induced by a viral protein that is related to plasma protein inhibitors of serine proteases.
- Induction of rat liver parenchymal cell apoptosis by hepatic myofibroblasts via transforming growth factor β
- Accumulation and cellular localization of fibrinogen/fibrin during short-term and long-term rat liver injury.
- Monoclonal antibody-mediated tumor regression by induction of apoptosis.
- Prevention of Apoptosis by Bcl-2: Release of Cytochrome c from Mitochondria Blocked
- Cytolytic T-cell cytotoxicity is mediated through perforin and Fas lytic pathways
- p53-Dependent apoptosis in the absence of transcriptional activation of p53-target genes
- An evolutionary perspective on apoptosis.
- The TNF receptor superfamily of cellular and viral proteins: activation, costimulation, and death.
- CD95 (Fas)-dependent elimination of self-reactive B cells upon interaction with CD4+T cells
- Multiple pathways to apoptosis.
- FADD/MORT1 Is a Common Mediator of CD95 (Fas/APO-1) and Tumor Necrosis Factor Receptor-induced Apoptosis (*)
- Lymphocyte apoptosis induced by CD95 (APO–1/Fas) ligand–expressing tumor cells — A mechanism of immune evasion?
- Cell death by apoptosis and its protective role against disease.
Cited by
- Mechanisms of spontaneous resolution of rat liver fibrosis. Hepatic stellate cell apoptosis and reduced hepatic expression of metalloproteinase inhibitors.
- Induction of apoptosis by tanshinone I via cytochrome c release in activated hepatic stellate cells.
- Growth inhibition and apoptosis in liver myofibroblasts promoted by hepatocyte growth factor leads to resolution from liver cirrhosis.
- Thiol redox systems and protein kinases in hepatic stellate cell regulatory processes
- Effects of interleukin-10 on activation and apoptosis of hepatic stellate cells in fibrotic rat liver.
- The role of FasL and Fas in health and disease.
- Effects of platelet-derived growth factor and interleukin-10 on Fas/Fas-ligand and Bcl-2/Bax mRNA expression in rat hepatic stellate cells in vitro.
- Fibrogenese Pathophysiologie und therapeutische Ansätze
- Immune mediated liver failure
- The use of a recombinant single chain antibody in the investigation of liver fibrosis
- Regulation of fibrosis by the immune system.
- Effects of Fas-mediated liver cell apoptosis on diethylnitrosamine-induced hepatocarcinogenesis in mice
- Atorvastatin induces apoptosis by a caspase-9-dependent pathway: an in vitro study on activated rat hepatic stellate cells
- Addressing liver fibrosis with lipid-based drug carriers targeted to hepatic stellate cells
- Apoptosis and Necrosis in the Liver
- Pathogenesis and reversal of liver fibrosis: Effects of genes and environment
- Experimental models of liver fibrosis
- Intracellular Regulation of Fas-Induced Apoptosis in Human Fibroblasts by Extracellular Factors and Cycloheximide 1
- Hepatic stellate cells undermine the allostimulatory function of liver myeloid dendritic cells via STAT3-dependent induction of IDO
- In Vitro and In Vivo Protection of Stellate Cells from Apoptosis by Leptin
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