Search results for "Hepatic fibrosis"

showing 10 items of 50 documents

Human amniotic stem cells improve hepatic microvascular dysfunction and portal hypertension in cirrhotic rats

2020

BACKGROUND AND AIMS Portal hypertension is the main consequence of cirrhosis, responsible for the complications defining clinical decompensation. The only cure for decompensated cirrhosis is liver transplantation, but it is a limited resource and opens the possibility of regenerative therapy. We investigated the potential of primary human amniotic membrane-derived mesenchymal stromal (hAMSCs) and epithelial (hAECs) stem cells for the treatment of portal hypertension and decompensated cirrhosis. METHODS In vitro: Primary liver sinusoidal endothelial cells (LSECs) and hepatic stellate cells (HSCs) from cirrhotic rats (chronic CCl4 inhalation) were co-cultured with hAMSCs, hAECs or vehicle for…

Liver CirrhosisPathologymedicine.medical_specialtyhAECCirrhosisplacentaPortal venous pressure03 medical and health sciences0302 clinical medicineHypertension PortalSettore BIO/13 - BIOLOGIA APPLICATAAnimalsHumansMedicineAmnion610 Medicine & healthHepatologymedicine.diagnostic_testbusiness.industryMicrocirculationStem Cellschronic liver diseaseportal hypertensionEndothelial CellsAmniotic stem cellsmedicine.diseaseRatsLiver030220 oncology & carcinogenesisHepatic stellate cellPortal hypertensionVascular Resistance030211 gastroenterology & hepatologyStem cellbusinessHepatic fibrosisLiver function testshAMSCLiver International
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Deletion of organic cation transporter Oct3 promotes hepatic fibrosis via upregulation of TGFβ

2019

Organic cation transporters (OCT) are responsible for the intracellular uptake and detoxification of a broad spectrum of endogenous and exogenous substrates. OCTs are downregulated in cholestasis, fibrosis, and hepatocellular carcinoma, but the underlying molecular mechanisms and downstream effects of OCT deletion are unknown. Oct3-knockout ( Oct3−/−; FVB.Slc22a3tm10pb) and wild-type (WT; FVB) mice were subject to escalating doses of carbon tetrachloride (CCl4) or thioacetamide (TAA) for 6 wk to induce advanced parenchymal liver fibrosis. Secondary biliary fibrosis was generated by bile duct ligation. Liver fibrosis was assessed by hydroxyproline determination, quantitative Sirius red morp…

Liver CirrhosisTranscriptional ActivationPhysiologySLC22A3Transforming Growth Factor beta1MiceDownregulation and upregulationFibrosisPhysiology (medical)medicineAnimalsInflammationMice KnockoutCholestasisOrganic cation transport proteinsHepatologybiologyChemistryLiver NeoplasmsGastroenterologymedicine.diseaseUp-RegulationGene Expression RegulationDisease ProgressionHepatocytesbiology.proteinCancer researchCatecholamine Plasma Membrane Transport ProteinsHepatic fibrosisOctamer Transcription Factor-3Transforming growth factorAmerican Journal of Physiology-Gastrointestinal and Liver Physiology
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Congenital Cystic Lesions of the Bile Ducts: Imaging-Based Diagnosis

2020

Congenital cystic lesions of the bile ducts represent a spectrum of liver and biliary system lesions, resulting from abnormal embryologic development of the ductal plate. These disorders include Caroli disease, choledochal cysts, autosomal dominant polycystic liver disease, congenital hepatic fibrosis, and biliary hamartomas. Each disorder carries a peculiar clinical presentation, prognosis, and risk of complications. Knowledge of radiological findings of fibropolycystic liver diseases is crucial for their appropriate detection and for differential diagnosis with other similar hepatic cystic lesions, in order to avoid relevant misdiagnosis. The aim of this review is to provide an illustrati…

Liver Cirrhosismedicine.medical_specialtyCaroli diseaseDigestive System DiseasesHamartomaCystic lesions030218 nuclear medicine & medical imagingDiagnosis Differential03 medical and health sciencesCystic lesion0302 clinical medicineMedicineHumansRadiology Nuclear Medicine and imagingCholedochal cystsFibropolycystic liver diseasemedicine.diagnostic_testbusiness.industryCystsPolycystic liver diseaseLiver DiseasesUltrasoundGenetic Diseases InbornMagnetic resonance imagingmedicine.diseaseCaroli DiseaseLiver030220 oncology & carcinogenesisCongenital hepatic fibrosisRadiologyDifferential diagnosisbusinessSettore MED/36 - Diagnostica Per Immagini E Radioterapia
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The Relevance of Noninvasive Tools To Assess Fibrosis in Non-Alcoholic Fatty Liver Disease.

2020

Non-alcoholic fatty liver disease (NAFLD) is a growing cause of chronic liver diseases worldwide, involving about 25% of people. NAFLD incorporates a large spectrum of pathological conditions, from simple steatosis to non-alcoholic steatohepatitis (NASH), cirrhosis and its complications include hepatic decompensation and hepatocellular carcinoma (HCC). This progression occurs, over many years, in an asymptomatic way, until advanced fibrosis appears. Thus, the differentiation of NASH from simple steatosis and identification of advanced hepatic fibrosis are key issues. To date, the histological assessment of fibrosis with liver biopsy is the gold standard, but obviously, invasiveness is the …

Liver Cirrhosismedicine.medical_specialtyCirrhosisCarcinoma HepatocellularBiopsyDiseaseGastroenterology03 medical and health sciences0302 clinical medicineFibrosisNon-alcoholic Fatty Liver DiseaseInternal medicineDrug DiscoverymedicineHumansPharmacologymedicine.diagnostic_testbusiness.industryFatty liverLiver Neoplasmsnutritional and metabolic diseasesBiomarkers FibroScan Fibrosis MRE MRI NAFLD NASH Non-invasive testsmedicine.diseasedigestive system diseasesLiver030220 oncology & carcinogenesisLiver biopsyHepatocellular carcinoma030211 gastroenterology & hepatologySteatohepatitisbusinessHepatic fibrosisCurrent pharmaceutical design
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Reading the stars for hepatic fibrosis or how to predict the severity of liver disease in patients with NASH

2018

BACKGROUND & AIMS: Non-invasive biomarkers are needed for monitoring changes in liver histology in patients with non-alcoholic steatohepatitis (NASH). Obeticholic acid (OCA) was shown to improve fibrosis in patients with NASH in the FLINT trial; a post hoc analysis of these data was performed to determine the relationship between 3 non-invasive fibrosis markers and liver fibrosis improvement. METHODS: In the Phase 2b FLINT trial, patients were randomised (1:1) to receive 25 mg OCA or placebo once daily for 72 weeks. Aspartate aminotransferase:platelet ratio index (APRI), fibrosis-4 (FIB-4) index, and non-alcoholic fatty liver disease fibrosis score (NFS) were evaluated in serum at baseline …

Liver Cirrhosismedicine.medical_specialtyHepatologybusiness.industrymedia_common.quotation_subjectMEDLINEmedicine.diseaseFibrosisGastroenterologyArticleLiver diseaseText miningReadingNon-alcoholic Fatty Liver DiseaseFibrosisReading (process)Internal medicinemedicineHumansIn patientHepatic fibrosisbusinessBiomarkersmedia_commonLiver International
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Liver fibrosis induced by hepatic overexpression of PDGF-B in transgenic mice

2006

Background/Aims In hepatic fibrogenesis, stellate cells are activated leading to production and deposition of extracellular matrix. To clarify the role of PDGF-B in liver fibrogenesis, we overexpressed PDGF-B in the liver of transgenic mice. Methods Transgenic mice for the conditional overexpression of PDGF-B in the liver under control of an albumin promoter were generated utilising the Cre/loxP system. Constitutive PDGF-B expression was achieved after breeding with mice expressing Cre-recombinase under actin promoter control. Tamoxifen inducible expression was achieved after breeding with mice expressing Cre under transthyretin receptor promoter control. Levels of fibrosis were assessed an…

Liver Cirrhosismedicine.medical_specialtyPlatelet-derived growth factorLiver cytologyTransgeneMice TransgenicBiologyMicechemistry.chemical_compoundTransforming Growth Factor betaFibrosisInternal medicinemedicineAnimalsPromoter Regions GeneticCells CulturedCell ProliferationIntegrasesHepatologyTransdifferentiationCell DifferentiationProto-Oncogene Proteins c-sisFibroblastsmedicine.diseaseExtracellular MatrixEndocrinologyGene Expression RegulationLiverchemistryHepatocytesCancer researchHepatic stellate cellHepatic fibrosisMyofibroblastJournal of Hepatology
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Neurotensin up-regulation is associated with advanced fibrosis and hepatocellular carcinoma in patients with MAFLD

2020

Background & aims: Neurotensin (NTS), a 13-aminoacid peptide localized in central nervous system and gastrointestinal tract, is involved in lipid metabolism and promotes various cancers onset mainly by binding to neurotensin receptor 1 (NTSR1). Increased plasma levels of pro-NTS, the stable NTS precursor, have been associated with type 2 diabetes (T2D), cardiovascular diseases and metabolic associated fatty liver disease (MAFLD). We aimed to evaluate 1) the impact of NTS rs1800832 and NTSR1 rs6090453 genetic variants on liver damage in 1166 MAFLD European individuals, 2) the relation between NTS variant and circulating pro-NTS and 3) the hepatic NTS expression by RNAseq transcriptomic a…

Male0301 basic medicineLiver damagemedicine.medical_specialtyGenetic variantsCarcinoma HepatocellularNeurotensin receptor 1CirrhosisTherapeutic targetSettore MED/12 - GASTROENTEROLOGIAType 2 diabetesGastroenterology03 medical and health sciencesLiver disease0302 clinical medicineFibrosisInternal medicinemedicineHumansReceptors NeurotensinBiomarker; Genetic variants; Lipid metabolism; Liver damage; Therapeutic targetMolecular BiologyNeurotensinAgedCell Proliferationbusiness.industryLiver NeoplasmsFatty liverBiomarker Genetic variants Lipid metabolism Liver damage Therapeutic targetCell BiologyBiomarkerMiddle Agedrespiratory systemmedicine.diseaseFibrosisFatty Liver030104 developmental biologyLipid metabolismDiabetes Mellitus Type 2Gene Expression Regulationnervous systemHepatocellular carcinomaMutationFemale030211 gastroenterology & hepatologybusinessHepatic fibrosiscirculatory and respiratory physiology
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Cholesterol burden in the liver induces mitochondrial dynamic changes and resistance to apoptosis

2018

Non-alcoholic fatty liver disease (NAFLD) encompasses a broad spectrum of histopathological changes ranging from non-inflammatory intracellular fat deposition to non-alcoholic steatohepatitis (NASH), which may progress into hepatic fibrosis, cirrhosis, or hepatocellular carcinoma. Recent data suggest that impaired hepatic cholesterol homeostasis and its accumulation are relevant to the pathogenesis of NAFLD/NASH. Despite a vital physiological function of cholesterol, mitochondrial dysfunction is an important consequence of dietary-induced hypercholesterolemia and was, subsequently, linked to many pathophysiological conditions. The aim in the current study was to evaluate the morphological a…

Male0301 basic medicinemedicine.medical_specialtyTime FactorsCirrhosisPhysiologyClinical BiochemistryApoptosisMitochondria LiverMitochondrionDiet High-Fatmedicine.disease_causeMitochondrial DynamicsCholesterol Dietary03 medical and health scienceschemistry.chemical_compound0302 clinical medicineNon-alcoholic Fatty Liver DiseaseInternal medicinemedicineAnimalsCells CulturedCell ProliferationCholesterolbusiness.industryFatty liverCell Biologymedicine.diseaseMice Inbred C57BLDisease Models AnimalOxidative Stress030104 developmental biologymedicine.anatomical_structureEndocrinologyGene Expression RegulationLiverchemistry030220 oncology & carcinogenesisHepatocyteHepatocytesSteatohepatitisTranscriptomeHepatic fibrosisbusinessOxidative stressJournal of Cellular Physiology
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Modulation of the gut microbiota impacts nonalcoholic fatty liver disease: A potential role for bile acids

2017

Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease worldwide, yet the pathogenesis of NAFLD is only partially understood. Here, we investigated the role of the gut bacteria in NAFLD by stimulating the gut bacteria via feeding mice the fermentable dietary fiber, guar gum (GG), and suppressing the gut bacteria via chronic oral administration of antibiotics. GG feeding profoundly altered the gut microbiota composition, in parallel with reduced diet-induced obesity and improved glucose tolerance. Strikingly, despite reducing adipose tissue mass and inflammation, GG enhanced hepatic inflammation and fibrosis, concurrent with markedly elevated plasma and hepatic bile acid l…

Male0301 basic medicineobesityGut floraGalactansGastroenterologyBiochemistryantibioticsMannansSTEATOHEPATITISVoeding Metabolisme en Genomicachemistry.chemical_compoundLiver diseaseEndocrinologyNon-alcoholic Fatty Liver DiseaseFibrosisAntibioticsPlant GumsNonalcoholic fatty liver diseaseHeptaic inflammationFIBROSIShepatic fibrosisResearch ArticlesHuman Nutrition & HealthbiologyBile acidHumane Voeding & GezondheidMetabolic Disorders Radboud Institute for Molecular Life Sciences [Radboudumc 6]Metabolism and GenomicsAnti-Bacterial Agents3. Good healthIntestineL-CARNITINELiverGUAR GUM[ SDV.BBM.GTP ] Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]Metabolisme en Genomica[SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]Nutrition Metabolism and Genomics[ SDV.MHEP.HEG ] Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterologymedicine.medical_specialtymedicine.drug_classBiochemieCelbiologie en ImmunologieQD415-436Gut microbiotaMETABOLISMDiet High-Fatdigestive systemDIET03 medical and health sciencesVoedingINFLAMMATIONINTESTINAL MICROBIOTAInternal medicine[SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]medicineAnimalsHepatic inflammationObesityintestineVLAGNutritionInflammationBile acids and saltshepatic inflammationBiological Transport[SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyCell BiologyGlucose Tolerance Testmedicine.diseaseTaurocholic acidbiology.organism_classification[SDV.MHEP.HEG] Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyGastrointestinal MicrobiomeMice Inbred C57BLMICE030104 developmental biologyEndocrinologychemistryCell Biology and ImmunologySteatohepatitisHepatic fibrosisTRIMETHYLAMINE-N-OXIDEHepatic fibrosis
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TIMP expression in toxic and cholestatic liver injury in rat.

1997

Abstract Background/Aims: Hepatic fibrosis is a dynamic pathological process with a net accumulation of extracellular matrix proteins. Recent evidence suggests that besides their increased synthesis, inhibition of matrix degradation plays a significant role. ECM degradation occurs via metalloproteinases which are inhibited in situ by specific tissue inhibitors of metalloproteinases (TIMPs). The aim of our studies was to determine the expression of TIMPs during toxic liver injury and cholestatic liver injury leading to fibrosis. Methods: We examined the expression of TIMP-1, -2 and -3 in two different rat models for liver injury (intraperitoneal CCl 4 injection and bile duct ligation) by Nor…

MalePathologymedicine.medical_specialtyIn situ hybridizationCholestasis IntrahepaticMatrix metalloproteinaseBiologyRats Sprague-DawleyCholestasisFibrosisInternal medicinemedicineAnimalsNorthern blotIn Situ HybridizationLiver injuryTissue Inhibitor of Metalloproteinase-3Tissue Inhibitor of Metalloproteinase-2Tissue Inhibitor of Metalloproteinase-1HepatologyCarbon Tetrachloride PoisoningAcute-phase proteinTissue Inhibitor of Metalloproteinasesmedicine.diseaseRatsEndocrinologyLiverChemical and Drug Induced Liver InjuryHepatic fibrosisJournal of hepatology
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