2014
Pathophysiology of Portal Hypertension
Iwakiri Y. Pathophysiology of Portal Hypertension. Clinics In Liver Disease 2014, 18: 281-291. PMID: 24679494, PMCID: PMC3971388, DOI: 10.1016/j.cld.2013.12.001.BooksConceptsPortal hypertensionBlood flowHyperdynamic circulatory syndromeIntrahepatic vascular resistancePortal blood flowVascular resistanceArterial vasodilationCirculatory syndromeEsophageal varicesLiver cirrhosisMajor complicationsLiver diseaseCollateral vesselsPortal circulationSystemic circulationHypertensionPathologic conditionsClinical researchCirrhosisVaricesVasodilationAscitesComplicationsPathophysiologySyndromePigment Epithelium-Derived Factor (PEDF) Suppresses IL-1β-Mediated c-Jun N-Terminal Kinase (JNK) Activation to Improve Hepatocyte Insulin Signaling
Gattu AK, Birkenfeld AL, Iwakiri Y, Jay S, Saltzman M, Doll J, Protiva P, Samuel VT, Crawford SE, Chung C. Pigment Epithelium-Derived Factor (PEDF) Suppresses IL-1β-Mediated c-Jun N-Terminal Kinase (JNK) Activation to Improve Hepatocyte Insulin Signaling. Endocrinology 2014, 155: 1373-1385. PMID: 24456163, PMCID: PMC5393334, DOI: 10.1210/en.2013-1785.Peer-Reviewed Original ResearchMeSH KeywordsAdipocytesAnimalsEye ProteinsGene Expression RegulationGlucose Tolerance TestHepatocytesHumansInflammationInsulinInsulin ResistanceInterleukin-1betaJNK Mitogen-Activated Protein KinasesLiverMaleMetabolic SyndromeMetabolomicsMiceMice, Inbred C57BLMice, KnockoutMicrospheresNerve Growth FactorsObesityPalmitic AcidPhenotypeRNA InterferenceSerpinsSignal TransductionSuccinic AcidConceptsPigment epithelium-derived factorKO miceMetabolic syndromeIL-1βC-Jun N-terminal kinase (JNK) activationElevated pigment epithelium-derived factorIL-1β challengeHuman hepatocytesIL-1β expressionHuman metabolic syndromeEpithelium-derived factorPEDF-knockout miceInflammatory markersGlucose intoleranceSerum levelsC-Jun N-terminal kinaseKinase activationAntiinflammatory proteinHepatic insulinKnockout micePigment epitheliumN-terminal kinaseMiceSyndromeMetabolic homeostasis
2008
Vascular biology and pathobiology of the liver: Report of a single‐topic symposium
Iwakiri Y, Grisham M, Shah V. Vascular biology and pathobiology of the liver: Report of a single‐topic symposium. Hepatology 2008, 47: 1754-1763. PMID: 18393322, PMCID: PMC2724750, DOI: 10.1002/hep.22203.BooksConceptsPortal hypertensionVascular biologyIschemia-reperfusion injurySingle Topic ConferenceMajority of morbidityClinical sequelaeIR injurySpecific disease syndromesLiver diseaseVascular syndromesVascular diseaseVascular cell signalingHypertensionDisease syndromeLiver cellsSyndromeMajor vascular defectsLiverVascular defectsInjuryDiseasePathobiologyAmerican AssociationCell signalingCirrhosis
2006
The hyperdynamic circulation of chronic liver diseases: From the patient to the molecule
Iwakiri Y, Groszmann RJ. The hyperdynamic circulation of chronic liver diseases: From the patient to the molecule. Hepatology 2006, 43: s121-s131. PMID: 16447289, DOI: 10.1002/hep.20993.BooksMeSH KeywordsAdrenomedullinAnimalsBiological FactorsBlood PressureCannabinoid Receptor ModulatorsCarbon MonoxideChronic DiseaseDisease Models, AnimalEndothelium, VascularHumansHydrogen SulfideHypertension, PortalLiverLiver DiseasesNitric OxidePeptidesSplanchnic CirculationTumor Necrosis Factor-alphaVasodilationConceptsHyperdynamic circulatory syndromeChronic liver diseaseCirculatory syndromeLiver diseaseVasodilator moleculeClinical observationsExperimental modelComplex pathophysiological mechanismsHyperdynamic circulationProgressive vasodilatationPortal hypertensionPathophysiological mechanismsVascular abnormalitiesComplex syndromeMultiple organsPatientsNitric oxideSyndromeVasodilatationDiseaseDetrimental effectsHypertensionAbnormalitiesComplex mechanisms
2004
The paradox: vasoconstriction and vasodilation
Iwakiri Y, Groszmann R. The paradox: vasoconstriction and vasodilation. 2004, 57-67. DOI: 10.1007/978-94-007-1042-9_7.Peer-Reviewed Original ResearchPortal hypertensionLiver diseaseVascular toneNitric oxideHyperdynamic circulatory syndromeChronic liver diseaseHomeostatic mechanismsBody's homeostatic mechanismsCirculatory syndromeImpaired oxygenationElectrolyte imbalanceHomeostatic functionsKey moleculesHypertensionProgressive alterationDiseaseToneVasoconstrictionVasodilationPatientsPatients1Major rolePathogenesisSyndromeAbnormalities