2023
Humanized mouse liver reveals endothelial control of essential hepatic metabolic functions
Kaffe E, Roulis M, Zhao J, Qu R, Sefik E, Mirza H, Zhou J, Zheng Y, Charkoftaki G, Vasiliou V, Vatner D, Mehal W, AlcHepNet, Kluger Y, Flavell R. Humanized mouse liver reveals endothelial control of essential hepatic metabolic functions. Cell 2023, 186: 3793-3809.e26. PMID: 37562401, PMCID: PMC10544749, DOI: 10.1016/j.cell.2023.07.017.Peer-Reviewed Original ResearchConceptsMetabolic functionsSpecies-specific interactionsKey metabolic functionsCell-autonomous mechanismsNon-alcoholic fatty liver diseaseMajor metabolic hubNon-parenchymal cellsMetabolic hubHuman hepatocytesMicroenvironmental regulationHuman diseasesHuman-specific aspectsHuman pathologiesHomeostatic processesSpecies mismatchCholesterol uptakeFatty liver diseaseParacrine mannerHuman immuneBile acid conjugationSinusoidal endothelial cellsHepatic metabolic functionMouse liverEndothelial cellsCells
2018
Role of sterile inflammation in fatty liver diseases
Chen Y, Yousaf M, Mehal W. Role of sterile inflammation in fatty liver diseases. Liver Research 2018, 2: 21-29. DOI: 10.1016/j.livres.2018.02.003.Peer-Reviewed Original ResearchNon-alcoholic steatohepatitisSterile inflammationInflammatory responseTissue damageRegulatory T cellsFatty liver diseaseAnti-inflammatory effectsHepatic inflammatory responseAcute phase reactantsHigh-fat dietPropagation of inflammationSinusoidal endothelial cellsPro-inflammatory damageTrans retinoic acidGrowth factor βLiver inflammationMetabolic syndromeLiver diseaseIL-1βInflammatory cytokinesFat dietAlcohol excessFemale micePhase reactantsT cells
2009
Acetaminophen-induced hepatotoxicity in mice is dependent on Tlr9 and the Nalp3 inflammasome
Imaeda AB, Watanabe A, Sohail MA, Mahmood S, Mohamadnejad M, Sutterwala FS, Flavell RA, Mehal WZ. Acetaminophen-induced hepatotoxicity in mice is dependent on Tlr9 and the Nalp3 inflammasome. Journal Of Clinical Investigation 2009, 119: 305-314. PMID: 19164858, PMCID: PMC2631294, DOI: 10.1172/jci35958.Peer-Reviewed Original ResearchMeSH KeywordsAcetaminophenAnalgesics, Non-NarcoticAnimalsApoptosisAspirinCarrier ProteinsCaspase InhibitorsCell LineCyclooxygenase InhibitorsDose-Response Relationship, DrugHumansImmunity, InnateInflammationInterleukin-18Interleukin-1betaLiverMiceMice, Inbred C57BLNLR Family, Pyrin Domain-Containing 3 ProteinSignal TransductionToll-Like Receptor 9ConceptsLiver injuryIL-1betaNALP3 inflammasomeHepatocyte deathAcetaminophen-induced liver injuryCaspase-1Proinflammatory cytokine activationInnate immune activationSterile inflammatory responseType of injuryCOX-1 inhibitionMature IL-1betaPotential therapeutic approachSinusoidal endothelial cellsOverall tissue injuryIL-18Immune activationProinflammatory cytokinesTLR9 antagonistInitial insultInflammatory responseTissue injuryProtective effectCytokine activationTherapeutic approaches
1999
Selective retention of activated CD8+ T cells by the normal liver.
Mehal W, Juedes A, Crispe I. Selective retention of activated CD8+ T cells by the normal liver. The Journal Of Immunology 1999, 163: 3202-10. PMID: 10477588, DOI: 10.4049/jimmunol.163.6.3202.Peer-Reviewed Original Research