Search results for "liver injury"

showing 10 items of 144 documents

Dominant negative MORT1/FADD rescues mice from CD95 and TNF-induced liver failure

2002

Derangement of the apoptotic program is considered an important cause of liver disease. It became clear that receptor-mediated apoptosis is of specific interest in this context, and CD95 and CD120a, both members of the tumor necrosis factor (TNF) receptor superfamily, are the most prominent cell death receptors involved. The death signal is induced upon ligand binding by recruitment of caspases via the adapter molecule MORT1/FADD to the receptor and their subsequent activation. To investigate the role of MORT1/FADD in hepatocyte apoptosis, we generated transgenic mice expressing liver-specific dominant negative mutant. Mice looked grossly normal; breeding and liver development were not diff…

Lipopolysaccharidesmedicine.medical_specialtyProgrammed cell deathFas-Associated Death Domain ProteinOligonucleotidesMice TransgenicAntibodiesReceptors Tumor Necrosis FactorMiceLiver diseaseAntigens CDAlbuminsInternal medicinemedicineAnimalsfas ReceptorFADDPromoter Regions GeneticAdaptor Proteins Signal TransducingLiver injuryHepatitisMice Inbred BALB CHepatologybiologyTumor Necrosis Factor-alphamedicine.diseaseFas receptorMice Inbred C57BLEndocrinologyReceptors Tumor Necrosis Factor Type IApoptosisCaspasesbiology.proteinTumor necrosis factor alphaCarrier ProteinsLiver FailureHepatology
researchProduct

Dendritic cells in liver injury and fibrosis: shortcomings and promises.

2013

SummaryThe phenotype and function of liver dendritic cells (LDCs) are poorly understood. This Snapshot summarizes our current knowledge on LDCs in the healthy and injured liver, and their role in fibrosis progression and reversal. It also draws attention to various pitfalls in the current experimental design and conclusions based on available data.

Liver CirrhosisLiver dendritic cellsPlasmacytoid dendritic cellBiologyCCL2MiceFMS-like tyrosine kinase 3 ligandFibrosismedicineAnimalsHumansAntigen-presenting cellLiver injuryHepatologyFlt3LDendritic Cellsmedicine.diseaseCD11c-DTRDisease Models Animalmedicine.anatomical_structurePhenotypeLiverImmunologyHepatic stellate cellDisease ProgressionBone marrowToleranceJournal of hepatology
researchProduct

Collagen biology and non‐invasive biomarkers of liver fibrosis

2020

There is an unmet need for high-quality liquid biomarkers that can safely and reproducibly predict the stage of fibrosis and the outcomes of chronic liver disease (CLD). The requirement for such markers has intensified because of the high global prevalence of diseases such as non-alcoholic fatty liver disease (NAFLD). In particular, there is a need for diagnostic and prognostic tools, as well as predictive biomarkers that reflect the efficacy of interventions, as described by the BEST criteria (Biomarkers, EndpointS, and other Tools Resource). This review covers the various liver collagens, their functional role in tissue homeostasis and delineates the common nomenclature for biomarkers bas…

Liver CirrhosisLiver injuryCirrhosisHepatologyFatty liverDiseaseBiologyBioinformaticsmedicine.diseaseChronic liver disease03 medical and health sciences0302 clinical medicineLiverNon-alcoholic Fatty Liver DiseaseFibrosis030220 oncology & carcinogenesismedicineHumansBiomarker (medicine)030211 gastroenterology & hepatologyCollagenBiologyBiomarkersTissue homeostasisLiver International
researchProduct

Increased hepatic fibrosis and JNK2-dependent liver injury in mice exhibiting hepatocyte-specific deletion of cFLIP.

2012

Chronic liver disease promotes hepatocellular injury involving apoptosis and triggers compensatory regeneration that leads to the activation of quiescent stellate cells in the liver. The deposition of extracellular matrix from activated myofibroblasts promotes hepatic fibrosis and the progression to cirrhosis with deleterious effects on liver physiology. The role of apoptosis signaling pathways in the development of fibrosis remains undefined. The aim of the current study was to determine the involvement of the caspase-8 homologue cellular FLICE-inhibitory protein (cFLIP) during the initiation and progression of fibrosis. Liver injury and fibrosis from carbon tetrachloride (CCl4) and thioa…

Liver CirrhosisMalePathologymedicine.medical_specialtyTime FactorsGenotypePhysiologyCASP8 and FADD-Like Apoptosis Regulating ProteinApoptosisBiologyThioacetamideChronic liver diseaseMicePhysiology (medical)medicineAnimalsMitogen-Activated Protein Kinase 9PhosphorylationExtracellular Signal-Regulated MAP KinasesCarbon TetrachlorideCompensatory regenerationLiver injuryMice KnockoutHepatologyCaspase 3Gastroenterologymedicine.diseaseCaspase 9Enzyme ActivationDisease Models Animalmedicine.anatomical_structurePhenotypeLiverApoptosisHepatocyteHepatic stellate cellCancer researchDisease ProgressionHepatocytesHepatocellular injuryChemical and Drug Induced Liver InjuryHepatic fibrosisSignal TransductionAmerican journal of physiology. Gastrointestinal and liver physiology
researchProduct

Genetic variation in the TLL1 gene is not associated with fibrosis in patients with metabolic associated fatty liver disease.

2020

Metabolic associated fatty liver disease (MAFLD) is the most prevalent liver disease in Western nations, with high heritability. A recent study of Japanese patients with the disease suggested that TLL1 rs17047200 is associated with fibrosis; whether a similar association is observed in Caucasian patients with MAFLD is unknown. We investigated the association of the TLL1 rs17047200 polymorphism with liver fibrosis in a cohort of Caucasian patients with MAFLD (n = 728). We also investigated whether TLL1 expression is altered during liver injury in humans, in murine models of fibrosis, and in in-vitro. While TLL1 expression is upregulated in the liver of humans with MAFLD and in mice, the rs17…

Liver CirrhosisMaleSteatosisGene ExpressionDiseasePathology and Laboratory MedicineInbred C57BLGastroenterologyPathogenesisCytopathologyCohort StudiesLiver diseaseMice0302 clinical medicineFibrosisMedicine and Health SciencesLiver injury0303 health sciencesMultidisciplinaryLiver DiseasesQFatty liverRTLL1Single NucleotideMiddle Aged3. Good healthUp-RegulationAdult; Animals; Cohort Studies; Fatty Liver; Female; Genetic Variation; Humans; Liver Cirrhosis; Male; Mice; Mice Inbred C57BL; Middle Aged; Tolloid-Like Metalloproteinases; Up-Regulation; Polymorphism Single NucleotideMedicineLiver Fibrosis030211 gastroenterology & hepatologyFemaleAnatomyResearch ArticleAdultmedicine.medical_specialtyHistologyTolloid-Like MetalloproteinasesSettore MED/12 - GASTROENTEROLOGIAScienceGastroenterology and HepatologyPolymorphism Single Nucleotide03 medical and health sciencesInternal medicinemedicineGeneticsAnimalsHumansPolymorphism030304 developmental biologyNutritionbusiness.industryAdult Animals Cohort Studies Fatty Liver Female Genetic Variation Humans Liver Cirrhosis Male Mice Mice Inbred C57BL Middle Aged Tolloid-Like Metalloproteinases Up-Regulation Polymorphism Single NucleotideBiology and Life SciencesGenetic Variationmedicine.diseaseFibrosisDietFatty LiverMice Inbred C57BLn/aAnatomical PathologySteatosisbusinessDevelopmental Biology
researchProduct

Should cirrhosis change our attitude towards treating non-hepatic cancer?

2011

Cirrhosis is a major cause of morbidity and mortality and is the end stage of any chronic liver disease. Cancer, a leading cause of death worldwide, is a growing global health issue. There are limited data in the literature on the incidence, prevalence and management of non-hepatic cancers (NHC) in cirrhotic patients. The aim of this brief review was to underline the main concerns, pitfalls and warnings regarding practice for these patients. Survival of patients with compensated cirrhosis is significantly longer than that of decompensated cirrhosis and patients with NHC and in Child-Pugh class C should not be candidates for cytotoxic chemotherapy. It is important before starting cytotoxic c…

Liver CirrhosisMalemedicine.medical_specialtyCirrhosisAntineoplastic AgentsComorbidityChronic liver diseaseGastroenterologyLiver diseaseInternal medicineCause of DeathNeoplasmsmedicineHumansIntensive care medicineSurvival rateCause of deathHepatologybusiness.industryPatient SelectionCancerProfessional Practicemedicine.diseasechemotherapy – cirrhosis – hepatotoxicity – non-hepatic cancerClinical trialSurvival RateClinical Trials Phase III as TopicPortal hypertensionFemaleChemical and Drug Induced Liver InjurybusinessLiver international : official journal of the International Association for the Study of the Liver
researchProduct

Impact of antithrombin III on hepatic and intestinal microcirculation in experimental liver cirrhosis and bowel inflammation: An in vivo analysis

2005

AIM: To analyze the hepatic and intestinal microcirculation in an animal model of liver cirrhosis and inflammatory bowel disease (IBD) and to characterize the anti-inflammatory action of antithrombin III (ATIII) on leukocyte kinetics and liver damage. METHODS: Hepatic and intestinal microcirculation was investigated by intravital videomicroscopy. Standardized models of experimental chronic liver cirrhosis and bowel inflammation were employed. Animals were divided into four groups (n = 6/group): controls, animals with cirrhosis, animals with cirrhosis and IBD, animals with cirrhosis and IBD treated with ATIII. RESULTS: Cirrhosis facilitated leukocyte rolling and sticking in hepatic sinusoids…

Liver CirrhosisMalemedicine.medical_specialtyCirrhosisSerine Proteinase InhibitorsAntithrombin IIIInflammationInflammatory bowel diseaseGastroenterologyMicrocirculationEnteritisInternal medicineMedicineAnimalsRats WistarLiver injurybusiness.industryMicrocirculationAntithrombinGastroenterologyGeneral MedicineBlood flowmedicine.diseasedigestive system diseasesEnteritisRatsIntestinesLiverBrief Reportsmedicine.symptombusinessmedicine.drug
researchProduct

Liver eosinophilic infiltrate is a significant finding in patients with chronic hepatitis C.

2008

Eosinophilic infiltrate of liver tissue is described in primary cholestatic diseases, hepatic allograft rejection and drug-induced liver injury, but its significance and its implications in chronic hepatitis C are unknown. The aim of this study was to investigate the clinical significance of eosinophilic liver infiltrate in patients with chronic hepatitis C. We retrospectively evaluated 147 patients with chronic hepatitis C. The presence of eosinophilic infiltrate was investigated in liver biopsies, and a numeric count of eosinophilic leucocytes in every portal tract was assessed. An eosinophilic infiltrate of liver tissue (> or =3 cells evaluated in the portal / periportal spaces) was obse…

Liver CirrhosisMalemedicine.medical_specialtyPathologyLiver steatosisSettore MED/08 - Anatomia PatologicaChronic hepatitis CGastroenterologyFibrosisVirologyInternal medicineEosinophiliaEosinophilicHumansMedicineClinical significanceRetrospective StudiesLiver injuryHepatologymedicine.diagnostic_testbusiness.industryLiver fibrosiOdds ratioHepatitis CHepatitis C ChronicLiver biopsymedicine.diseaseEosinophilsFatty LiverInfectious DiseasesLiverLiver biopsyFemaleEosinophilic infiltrateSteatosisDrugChronic hepatitis C; Drugs; Eosinophilic infiltrate; Liver biopsy; Liver fibrosis; Liver steatosisbusiness
researchProduct

Rilpivirine attenuates liver fibrosis through selective STAT1-mediated apoptosis in hepatic stellate cells

2020

ObjectiveLiver fibrosis constitutes a major health problem worldwide due to its rapidly increasing prevalence and the lack of specific and effective treatments. Growing evidence suggests that signalling through cytokine-activated Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathways regulates liver fibrosis and regeneration. Rilpivirine (RPV) is a widely used anti-HIV drug not reported to produce hepatotoxicity. We aimed to describe the potential hepatoprotective effects of RPV in different models of chronic liver injury, focusing on JAK-STAT signalling regulation.DesignThe effects of RPV on hepatic steatosis, inflammation and fibrogenesis were studied in a nut…

Liver CirrhosisSTAT3 Transcription Factor0301 basic medicineApoptosisRisk AssessmentSensitivity and SpecificityMice03 medical and health sciences0302 clinical medicineNon-alcoholic Fatty Liver DiseaseFibrosisHepatic Stellate CellsmedicineAnimalsHumansSTAT1610 Medicine & healthSTAT3Cells CulturedLiver injurybiologybusiness.industryRilpivirineFatty liverGastroenterologymedicine.diseaseLiver regenerationLiver RegenerationDisease Models AnimalSTAT1 Transcription FactorTreatment Outcome030104 developmental biology030220 oncology & carcinogenesisbiology.proteinHepatic stellate cellCancer researchbusinessJanus kinase
researchProduct

The lipid lowering drug lovastatin protects against doxorubicin-induced hepatotoxicity.

2012

Liver is the main detoxifying organ and therefore the target of high concentrations of genotoxic compounds, such as environmental carcinogens and anticancer drugs. Here, we investigated the usefulness of lovastatin, which is nowadays widely used for lipid lowering purpose, as a hepatoprotective drug following the administration of the anthracycline derivative doxorubicin in vivo. To this end, BALB/c mice were exposed to either a single high dose or three consecutive low doses of doxorubicin. Acute and subacute hepatotoxicities were analyzed with or without lovastatin co-treatment. Lovastatin protected the liver against doxorubicin-induced acute pro-inflammatory and pro-fibrotic stress respo…

Liver CirrhosisStatinAnthracyclinemedicine.drug_classBiologyPharmacologyToxicologymedicine.disease_causeMiceFibrosispolycyclic compoundsmedicineAnimalsDoxorubicinLovastatinRNA MessengerEpirubicinPharmacologyInflammationMice Inbred BALB CAntibiotics AntineoplasticDose-Response Relationship DrugConnective Tissue Growth Factormedicine.diseaseOxidative StressHepatoprotectionGene Expression RegulationDoxorubicinHMG-CoA reductasebiology.proteinlipids (amino acids peptides and proteins)LovastatinChemical and Drug Induced Liver InjuryHydroxymethylglutaryl-CoA Reductase InhibitorsOxidative stressmedicine.drugDNA DamageToxicology and applied pharmacology
researchProduct