Featured Publications
Hepatic lymphatic vascular system in health and disease
Jeong J, Tanaka M, Iwakiri Y. Hepatic lymphatic vascular system in health and disease. Journal Of Hepatology 2022, 77: 206-218. PMID: 35157960, PMCID: PMC9870070, DOI: 10.1016/j.jhep.2022.01.025.Peer-Reviewed Original ResearchConceptsLiver diseaseNon-alcoholic fatty liver diseaseLymphatic systemFatty liver diseaseCongenital liver diseasesPotential therapeutic strategyHepatic lymphatic systemLiver transplantationPortal hypertensionMalignant tumorsTherapeutic strategiesDisease pathogenesisHepatic physiologyDiseasePathological conditionsSpecific markersLymphatic vesselsVascular systemLymphatic vascular systemOrgansTissue homeostasisHypertensionTransplantationPathophysiologyPathogenesis
2024
Carbon monoxide-loaded red blood cells ameliorate metabolic dysfunction-associated steatohepatitis progression via enhancing AMP-activated protein kinase activity and inhibiting Kupffer cell activation
Yanagisawa H, Maeda H, Noguchi I, Tanaka M, Wada N, Nagasaki T, Kobayashi K, Kanazawa G, Taguchi K, Chuang V, Sakai H, Nakashima H, Kinoshita M, Kitagishi H, Iwakiri Y, Sasaki Y, Tanaka Y, Otagiri M, Watanabe H, Maruyama T. Carbon monoxide-loaded red blood cells ameliorate metabolic dysfunction-associated steatohepatitis progression via enhancing AMP-activated protein kinase activity and inhibiting Kupffer cell activation. Redox Biology 2024, 76: 103314. PMID: 39163766, PMCID: PMC11381851, DOI: 10.1016/j.redox.2024.103314.Peer-Reviewed Original ResearchAMP-activated protein kinaseKupffer cell activationHeme oxygenase-1Red blood cellsInhibit Kupffer cell activationLiver heme oxygenase-1Suppress Kupffer cell activationCell activationLiver regenerationModel miceBlood cellsFat accumulationActivating AMP-activated protein kinaseAMP-activated protein kinase activationImpaired liver regenerationMethionine-choline deficient dietNonalcoholic fatty liver diseaseRestore liver regenerationFatty liver diseaseReceptor inductionHealthy miceProtein kinase activityPromoting fatty acid oxidationMouse modelLiver disease
2020
Reduced Nogo expression inhibits diet-induced metabolic disorders by regulating ChREBP and insulin activity
Zhang S, Guo F, Yu M, Yang X, Yao Z, Li Q, Wei Z, Feng K, Zeng P, Zhao D, Li X, Zhu Y, Miao QR, Iwakiri Y, Chen Y, Han J, Duan Y. Reduced Nogo expression inhibits diet-induced metabolic disorders by regulating ChREBP and insulin activity. Journal Of Hepatology 2020, 73: 1482-1495. PMID: 32738448, DOI: 10.1016/j.jhep.2020.07.034.Peer-Reviewed Original ResearchConceptsDiet-induced metabolic disordersHepatic lipid accumulationInsulin sensitivityMetabolic disordersInsulin resistanceNogo expressionNon-alcoholic fatty liver diseaseDiet-induced body weight gainInsulin activityDiet-induced glucose intoleranceLipid accumulationFatty liver diseaseHigh-fructose dietGrowth factor 21Littermate control miceDe novo lipogenesisHigh-carbohydrate dietBody weight gainCarbohydrate-responsive element-binding proteinExpression of ChREBPChREBP activityEndoplasmic reticulum stressMetabolic complicationsGlucose intoleranceLiver disease
2015
Nonalcoholic fatty liver disease induced by noncanonical Wnt and its rescue by Wnt3a
Wang S, Song K, Srivastava R, Dong C, Go G, Li N, Iwakiri Y, Mani A. Nonalcoholic fatty liver disease induced by noncanonical Wnt and its rescue by Wnt3a. The FASEB Journal 2015, 29: 3436-3445. PMID: 25917329, PMCID: PMC4511193, DOI: 10.1096/fj.15-271171.Peer-Reviewed Original ResearchMeSH KeywordsActinsAnimalsCell Line, TumorCell TransdifferentiationFatty LiverHep G2 CellsHepatocytesHumansLiverLow Density Lipoprotein Receptor-Related Protein-6MiceMice, Inbred C57BLNon-alcoholic Fatty Liver DiseaseProtein BindingProtein Kinase CProtein Kinase C-alphaRho-Associated KinasesSignal TransductionTransforming Growth Factor beta1VimentinWnt Signaling PathwayWnt3A ProteinConceptsNonalcoholic fatty liver diseaseFatty liver diseaseNonalcoholic steatohepatitisLiver diseaseLDL receptor-related protein 6NASH-related liver diseaseMetabolic risk factorsChronic liver diseaseEarly-onset atherosclerosisImportant potential therapeutic targetTGF-β1 activityPotential therapeutic targetDisease pathwaysRas homolog family member ASmooth muscle αFamily member ARisk factorsDisease progressionCommon causeLRP6 knockdownTherapeutic targetWnt3a administrationHepatocyte transdifferentiationDiseaseMuscle α