Search results for "cirrhosis"

showing 10 items of 964 documents

Determinants of fibrosis progression and regression in NASH

2017

Cirrhosis has become the major liver-related clinical endpoint in non-alcoholic steatohepatitis (NASH). However, progression to cirrhosis is less predictable in NASH than in other chronic liver diseases. This is due to the complex and multifactorial aetiology of NASH, which is determined by lifestyle and nutrition, multiple genetic and epigenetic factors, and a prominent role of hepatic and extrahepatic comorbidities. Thus, modest changes in these cofactors can also induce fibrosis regression, at least in patients with precirrhotic liver disease. Fibrogenesis in NASH correlates with, but is indirectly coupled to, classical inflammation, since fibrosis progression is driven by repetitive per…

0301 basic medicineLiver CirrhosisCirrhosisInflammationBioinformaticsCholangiocyte03 medical and health sciencesLiver disease0302 clinical medicineFibrosisNon-alcoholic Fatty Liver DiseaseClinical endpointMedicineHumansHepatologybusiness.industryDisease Managementmedicine.diseasePrognosis3. Good health030104 developmental biologyImmunologyHepatic stellate cellDisease Progression030211 gastroenterology & hepatologySteatohepatitismedicine.symptombusinessJournal of Hepatology
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Transcriptomic profiling across the nonalcoholic fatty liver disease spectrum reveals gene signatures for steatohepatitis and fibrosis

2020

International audience; The mechanisms that drive nonalcoholic fatty liver disease (NAFLD) remain incompletely understood. This large multicenter study characterized the transcriptional changes that occur in liver tissue across the NAFLD spectrum as disease progresses to cirrhosis to identify potential circulating markers. We performed high-throughput RNA sequencing on a discovery cohort comprising histologically characterized NAFLD samples from 206 patients. Unsupervised clustering stratified NAFLD on the basis of disease activity and fibrosis stage with differences in age, aspartate aminotransferase (AST), type 2 diabetes mellitus, and carriage of PNPLA3 rs738409 , a genetic variant assoc…

0301 basic medicineLiver CirrhosisCirrhosis[SDV]Life Sciences [q-bio]DiseaseBiologyTranscriptome03 medical and health sciences0302 clinical medicineFibrosisnashNon-alcoholic Fatty Liver DiseaseDiabetes mellitusNonalcoholic fatty liver diseasemedicineDiabetes MellitusHumansGeneral Medicinemedicine.disease3. Good health030104 developmental biologyDiabetes Mellitus Type 2LiverHumans; Liver; Liver Cirrhosis; Transcriptome; Diabetes Mellitus Type 2; Non-alcoholic Fatty Liver DiseaseImmunology030211 gastroenterology & hepatologyGDF15SteatohepatitisTranscriptomeType 2
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Hepatocyte pyroptosis and release of inflammasome particles induce stellate cell activation and liver fibrosis.

2019

Background & Aims Increased hepatocyte death contributes to the pathology of acute and chronic liver diseases. However, the role of hepatocyte pyroptosis and extracellular inflammasome release in liver disease is unknown. Methods We used primary mouse and human hepatocytes, hepatocyte-specific leucine 351 to proline Nlrp3KICreA mice, and GsdmdKO mice to investigate pyroptotic cell death in hepatocytes and its impact on liver inflammation and damage. Extracellular NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasomes were isolated from mutant NLRP3-YFP HEK cells and internalisation was studied in LX2 and primary human hepatic stellate cells. We also examined a cohort of 154…

0301 basic medicineLiver CirrhosisInflammasomesInterleukin-1betaArticle03 medical and health sciencesLiver diseaseMice0302 clinical medicineMice Inbred NODNon-alcoholic Fatty Liver DiseaseNLR Family Pyrin Domain-Containing 3 ProteinmedicineHepatic Stellate CellsPyroptosisAnimalsHumansLiver injuryHepatologyChemistryFatty liverCaspase 1PyroptosisInflammasomemedicine.disease3. Good healthCell biology030104 developmental biologymedicine.anatomical_structureHepatocyteHepatic stellate cellHepatocytesProtein Translocation Systems030211 gastroenterology & hepatologySteatohepatitisReactive Oxygen Speciesmedicine.drugJournal of hepatology
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Lysyl Oxidase (LOX) Family Members: Rationale and Their Potential as Therapeutic Targets for Liver Fibrosis.

2019

The cross-linking of structural extracellular matrix (ECM) components, especially fibrillar collagens and elastin, is strongly implicated in fibrosis progression and resistance to fibrosis reversal. Lysyl oxidase family members (LOX and LOXL1 [lysyl oxidase-like 1], LOXL2 [lysyl oxidase-like 2], LOXL3 [lysyl oxidase-like 3], and LOXL4 [lysyl oxidase like 4]) are extracellular copper-dependent enzymes that play a key role in ECM cross-linking, but have also other intracellular functions relevant to fibrosis and carcinogenesis. Although the expression of most LOX family members is elevated in experimental liver fibrosis of diverse etiologies, their individual contribution to fibrosis is incom…

0301 basic medicineLiver CirrhosisLysyl oxidaseExtracellular matrixProtein-Lysine 6-Oxidase03 medical and health sciences0302 clinical medicineFibrosisExtracellularmedicineAnimalsHumansLOXL3integumentary systemHepatologyLOXL2biologybusiness.industrymedicine.diseaseenzymes and coenzymes (carbohydrates)030104 developmental biologySimtuzumabCancer researchbiology.protein030211 gastroenterology & hepatologyAmino Acid OxidoreductasesbusinessElastinHepatology (Baltimore, Md.)References
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Dietary components modulate the risk of hepatocellular carcinoma in cirrhotic patients.

2018

Abstract Eighty percent of hepatocellular carcinoma (HCC) cases occur after cirrhosis from various etiologies. The association between diet and cancer is well accepted, but the links with cirrhosis progression and HCC risk have been poorly investigated. However, we hypothesized that diet could be a modifiable preventive factor for HCC. Thus, the aim of our study was to explore the relationships between dietary factors and the risk of HCC in a population of cirrhotic patients. A total of 582 cirrhotic patients were studied: 401 without HCC (controls) and 181 with HCC (cases). These patients were recruited between 2008 and 2012 for the “CiRCE” case-control study conducted in six French univer…

0301 basic medicineLiver CirrhosisMale*Diet/adverse effectsCirrhosisEndocrinology Diabetes and MetabolismGastroenterologyFood groupchemistry.chemical_compound0302 clinical medicineEndocrinologyDiet and cancerRisk FactorsOdds RatioProspective StudiesProspective cohort study*Case-control studyeducation.field_of_studyNutrition and DieteticsLiver NeoplasmsMiddle Aged3. Good healthHepatocellular carcinomaFemale*Feeding Behavior*Hepatocellular carcinomaFranceLiver Neoplasms/etiology/*prevention and controlVitaminmedicine.medical_specialtyCarcinoma Hepatocellular*CirrhosisPopulation030209 endocrinology & metabolism*Diet03 medical and health sciencesHepatocellular/etiology/*prevention and controlInternal medicinemedicineDiabetes MellitusHumanseducationLiver Cirrhosis/complications/*diet therapyAged030109 nutrition & dieteticsbusiness.industryCarcinomaCase-control studyFeeding Behaviormedicine.diseaseDietLogistic ModelschemistryCase-Control StudiesbusinessEnergy Intake[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyNutrition research (New York, N.Y.)
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Nuclear Translocation of RELB Is Increased in Diseased Human Liver and Promotes Ductular Reaction and Biliary Fibrosis in Mice.

2019

Background & Aims Cholangiocyte proliferation and ductular reaction contribute to the onset and progression of liver diseases. Little is known about the role of the transcription factor nuclear factor-κB (NF-κB) in this process. We investigated the activities of the RELB proto-oncogene NF-κB subunit in human cholangiocytes and in mouse models of liver disease characterized by a ductular reaction. Methods We obtained liver tissue samples from patients with primary sclerosing cholangitis, primary biliary cholangitis, hepatitis B or C virus infection, autoimmune hepatitis, alcoholic liver disease, or without these diseases (controls) from a tissue bank in Germany. Tissues were analyzed by immu…

0301 basic medicineLiver CirrhosisMaleAlcoholic liver diseaseCholangiocyte proliferationAutoimmune hepatitisProto-Oncogene MasLiver diseaseMice0302 clinical medicineCarbon TetrachlorideCells CulturedRELBLiver DiseasesGastroenterologyMiddle Aged3. Good healthDeubiquitinating Enzyme CYLDCysteine EndopeptidasesProtein TransportLiverGene Knockdown TechniquesCytokines030211 gastroenterology & hepatologyFemaleCell activationAdultLymphotoxin-betaAdolescentCholangitis SclerosingPrimary sclerosing cholangitis03 medical and health sciencesYoung AdultLymphotoxin beta ReceptormedicineAnimalsHumansRNA MessengerParenchymal TissueAgedCell ProliferationCell NucleusHepatologybusiness.industryTranscription Factor RelBEpithelial CellsDicarbethoxydihydrocollidinemedicine.diseaseFibrosis030104 developmental biologyCancer researchLiver functionBile DuctsbusinessGastroenterology
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The membrane-bound O-acyltransferase domain-containing 7 variant rs641738 increases inflammation and fibrosis in chronic hepatitis B.

2017

Chronic hepatitis B (CHB) is characterized by hepatic inflammation that promotes progression to cirrhosis and predisposes to the development of hepatocellular carcinoma (HCC). Subtle interindividual genetic variation as well as viral and environmental factors interact to determine disease progression between individuals. Recently, the rs641738 membrane-bound O-acyltransferase domain-containing 7 (MBOAT7) polymorphism was demonstrated to influence histological liver damage in alcoholic liver disease, nonalcoholic fatty liver disease, and hepatitis C, but no data are available for CHB. We evaluated rs641738 influence on disease severity in a cohort of 1,101 patients with CHB. Forty-two patien…

0301 basic medicineLiver CirrhosisMaleAlcoholic liver diseaseCirrhosisSex FactorSeverity of Illness IndexCohort StudiesGene FrequencyFibrosisNon-alcoholic Fatty Liver DiseaseNonalcoholic fatty liver diseaseAge FactorProspective StudiesChronicMembrane ProteinMultivariate AnalysiAge FactorsHepatitis CSingle NucleotideMiddle AgedHepatitis BPrognosisHepatocellular carcinomaDisease ProgressionFemaleHumanAdultmedicine.medical_specialtyLogistic ModelPrognosiAcyltransferaseLiver CirrhosiAcetyltransferases; Acyltransferases; Adult; Age Factors; Cohort Studies; Confidence Intervals; Disease Progression; Female; Gene Frequency; Genetic Predisposition to Disease; Hepatitis B Chronic; Humans; Liver Cirrhosis; Logistic Models; Male; Membrane Proteins; Middle Aged; Multivariate Analysis; Non-alcoholic Fatty Liver Disease; Polymorphism Single Nucleotide; Prognosis; Prospective Studies; Risk Assessment; Severity of Illness Index; Sex FactorsPolymorphism Single NucleotideRisk Assessment03 medical and health sciencesHepatitis B ChronicSex FactorsSDG 3 - Good Health and Well-beingAcetyltransferasesInternal medicineAcetyltransferasemedicineConfidence IntervalsHumansGenetic Predisposition to DiseasePolymorphismHepatologybusiness.industryMembrane ProteinsHepatologymedicine.diseaseMinor allele frequencyProspective Studie030104 developmental biologyLogistic ModelsImmunologyMultivariate AnalysisCohort StudiebusinessConfidence IntervalAcyltransferasesHepatology (Baltimore, Md.)
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MBOAT7 rs641738 variant and hepatocellular carcinoma in non-cirrhotic individuals

2017

AbstractNonalcoholic fatty liver disease (NAFLD) represents an emerging cause of hepatocellular carcinoma (HCC), especially in non-cirrhotic individuals. The rs641738 C > T MBOAT7/TMC4 variant predisposes to progressive NAFLD, but the impact on hepatic carcinogenesis is unknown. In Italian NAFLD patients, the rs641738 T allele was associated with NAFLD-HCC (OR 1.65, 1.08–2.55; n = 765), particularly in those without advanced fibrosis (p < 0.001). The risk T allele was linked to 3’-UTR variation in MBOAT7 and to reduced MBOAT7 expression in patients without severe fibrosis. The number of PNPLA3, TM6SF2, and MBOAT7 risk variants was associated with NAFLD-HCC independently of clinical fa…

0301 basic medicineLiver CirrhosisMaleAlcoholic liver diseasePathologyCirrhosisliver diseasesGastroenterology0302 clinical medicineSettore BIO/13 - Biologia ApplicataNon-alcoholic Fatty Liver DiseaseRisk FactorsNonalcoholic fatty liver diseasefatty liver-disease; cirrhosis; liver cancer; hepatitis C; hepatocellular carcinoma; liver diseases; fibrosis; carcinogenesis; fatty liver; allelesHCCProspective cohort studySettore MED/12 - GastroenterologiaMultidisciplinaryLiver NeoplasmsQRhepatocellular carcinomaSingle NucleotideMiddle Aged3. Good healthItalyfatty liver-diseaseHepatocellular carcinomaCohortMedicine030211 gastroenterology & hepatologyFemalecarcinogenesisAcyltransferases; Adult; Aged; Carcinoma Hepatocellular; Female; Gene Expression Regulation; Genotype; Humans; Italy; Liver Cirrhosis; Liver Neoplasms; Male; Membrane Proteins; Middle Aged; Non-alcoholic Fatty Liver Disease; Polymorphism Single Nucleotide; Risk Factors; Alleles; Genetic Association Studies; Genetic Predisposition to Disease; Genetic VariationAdultmedicine.medical_specialtyCarcinoma HepatocellularGenotypeSciencePolymorphism Single NucleotideArticleliver cancer03 medical and health sciencesInternal medicinemedicineHumansGenetic Predisposition to DiseaseAllelePolymorphismAllelesGenetic Association Studiesfatty liverAgedSettore MED/06 - ONCOLOGIA MEDICAbusiness.industrycirrhosisfibrosisCarcinomaGenetic VariationMembrane ProteinsHepatocellularmedicine.diseasedigestive system diseases030104 developmental biologyGene Expression Regulationhepatitis CbusinessAcyltransferasesTM6SF2Scientific Reports
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Pharmacokinetics of a sustained release formulation of PDGFβ-receptor directed carrier proteins to target the fibrotic liver

2018

Liver fibrogenesis is associated with excessive production of extracellular matrix by myofibroblasts that often leads to cirrhosis and consequently liver dysfunction and death. Novel protein-based antifibrotic drugs show high specificity and efficacy, but their use in the treatment of fibrosis causes a high burden for patients, since repetitive and long-term parenteral administration is required as most proteins and peptides are rapidly cleared from the circulation. Therefore, we developed biodegradable polymeric microspheres for the sustained release of proteinaceous drugs. We encapsulated the drug carrier pPB-HSA, which specifically binds to the PDGF beta R that is highly upregulated on a…

0301 basic medicineLiver CirrhosisMaleCirrhosisPolymersLiver fibrosisPharmaceutical Science02 engineering and technologyPharmacologyMULTIBLOCK-COPOLYMERReceptor Platelet-Derived Growth Factor beta03 medical and health sciencesPharmacokineticsFibrosisIn vivomedicinein vitro in vivo correlationAnimalsControlled releaseFIBROSISBiodegradable polymeric microspheresDRUG-DELIVERYSerum AlbuminIN-VIVOMice KnockoutPOLYMERIC MICROSPHERESDrug CarriersINTERFERON-GAMMAChemistryProtein deliveryAlbuminPDGF beta-receptor targeted drug carrier021001 nanoscience & nanotechnologymedicine.diseaseControlled releaseIMPLANTSMicrospheresANTIFIBROTIC THERAPIESMice Inbred C57BLMICE030104 developmental biologyDelayed-Action PreparationsDrug delivery0210 nano-technologyDrug carrierGROWTH-FACTOR RECEPTOR
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Protein tyrosine phosphatase 1b deficiency protects against hepatic fibrosis by modulating nadph oxidases

2019

Inflammation is typically associated with the development of fibrosis, cirrhosis and hepatocellular carcinoma. The key role of protein tyrosine phosphatase 1B (PTP1B) in inflammatory responses has focused this study in understanding its implication in liver fibrosis. Here we show that hepatic PTP1B mRNA expression increased after bile duct ligation (BDL), while BDL-induced liver fibrosis was markedly reduced in mice lacking Ptpn1 (PTP1B−/−) as assessed by decreased collagen deposition and α-smooth muscle actin (α-SMA) expression. PTP1B−/− mice also showed a significant increase in mRNA levels of key markers of monocytes recruitment (Cd68, Adgre1 and Ccl2) compared to their wild-type (PTP1B+…

0301 basic medicineLiver CirrhosisMaleClinical BiochemistryGene ExpressionApoptosisBiochemistryMice0302 clinical medicineFibrosisTransforming Growth Factor betaRNA Small Interferinglcsh:QH301-705.5Liver injuryProtein Tyrosine Phosphatase Non-Receptor Type 1lcsh:R5-920NADPH oxidaseProtein tyrosine phosphatase 1BbiologyChemistryNOX4Bile duct ligationImmunohistochemistry3. Good healthNOX1Femalelcsh:Medicine (General)hormones hormone substitutes and hormone antagonistsResearch PaperBone marrow transplantationKupffer CellsLiver fibrosisdigestive systemCell LineBile Acids and Salts03 medical and health sciencesmedicineHepatic Stellate CellsAnimalsInflammationOrganic Chemistrymedicine.diseaseMolecular biologyTransplantationDisease Models Animal030104 developmental biologylcsh:Biology (General)Culture Media ConditionedNADPH oxidasesHepatic stellate cellbiology.proteinHepatocytesHepatic fibrosisReactive Oxygen Species030217 neurology & neurosurgeryBiomarkersRedox Biology
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