2025
Adding insult to injury: the spectrum of tubulointerstitial responses in acute kidney injury
Baker M, Cantley L. Adding insult to injury: the spectrum of tubulointerstitial responses in acute kidney injury. Journal Of Clinical Investigation 2025, 135: e188358. PMID: 40091836, PMCID: PMC11910233, DOI: 10.1172/jci188358.Peer-Reviewed Original ResearchConceptsAcute kidney injuryTubular epithelial cellsKidney injuryTubular cellsCases of acute kidney injuryImmune-mediated processPersistence of inflammationBiphasic immune responseChronic kidney diseaseCell deathTubular cell injuryLymphocyte subsetsTubular repairCell cycle arrestOutflow obstructionTEC differentiationPreclinical findingsLymphocytic infiltrationProinflammatory macrophagesKidney diseaseModulate inflammationImmune responseActivated macrophagesMetabolic reprogrammingTubular casts
2024
Analysis of Kidney Biopsies from Patients with Glomerulonephritis Using Imaging Mass Cytometry Reveals Increase in Immune Cells with Associated Dedifferentiation and Injury of Tubular Cells
Weiss M, Kakade V, Baker M, Budiman T, Shelar A, Cantley L. Analysis of Kidney Biopsies from Patients with Glomerulonephritis Using Imaging Mass Cytometry Reveals Increase in Immune Cells with Associated Dedifferentiation and Injury of Tubular Cells. Journal Of The American Society Of Nephrology 2024, 35: 10.1681/asn.202490mzwbkc. DOI: 10.1681/asn.202490mzwbkc.Peer-Reviewed Original ResearchPreventing MMP23-mediated cleavage of podocyte RARRES1: a novel strategy to halt chronic kidney disease progression?
Medina Rangel P, Ishibe S. Preventing MMP23-mediated cleavage of podocyte RARRES1: a novel strategy to halt chronic kidney disease progression? Kidney International 2024, 106: 16-18. PMID: 38906649, DOI: 10.1016/j.kint.2024.05.004.Peer-Reviewed Original Research
2022
Authors' Reply: Most Arginase-1 Positive Cells Are Likely Injured S3 Proximal Tubular Cells Carrying Upregulated Phagocytotic Capacity rather than M2 Macrophages—Too Many To Be True
Shin N, Marlier A, Xu L, Doilicho N, Linberg D, Guo J, Cantley L. Authors' Reply: Most Arginase-1 Positive Cells Are Likely Injured S3 Proximal Tubular Cells Carrying Upregulated Phagocytotic Capacity rather than M2 Macrophages—Too Many To Be True. Journal Of The American Society Of Nephrology 2022, 33: 2124-2125. PMID: 36316094, PMCID: PMC9678031, DOI: 10.1681/asn.2022070836.Peer-Reviewed Original ResearchArginase-1 Is Required for Macrophage-Mediated Renal Tubule Regeneration
Shin NS, Marlier A, Xu L, Doilicho N, Linberg D, Guo J, Cantley LG. Arginase-1 Is Required for Macrophage-Mediated Renal Tubule Regeneration. Journal Of The American Society Of Nephrology 2022, 33: 1077-1086. PMID: 35577558, PMCID: PMC9161787, DOI: 10.1681/asn.2021121548.Peer-Reviewed Original ResearchConceptsIschemia-reperfusion injuryTubular cell proliferationArginase-1Contralateral nephrectomyRenal repairFl/Littermate controlsTubular cellsReceptor 1GM-CSFRenal tubular cell proliferationRenal tubule regenerationMacrophage scavenger receptor 1Mannose receptor 1Cell proliferative responsesCell proliferationScavenger receptor 1Coculture of macrophagesDead cell debrisKidney injuryKidney repairRenal responseProinflammatory activationTubule regenerationMouse survivalInfiltrative Disease of the Tubulointerstitium
Aklilu A, Luciano R. Infiltrative Disease of the Tubulointerstitium. 2022, 231-241. DOI: 10.1007/978-3-030-93438-5_18.Peer-Reviewed Original ResearchInfiltrative diseasePlasma cell disordersRenal cell carcinomaRenal tubular cellsWhite blood cellsCancer-targeted therapyKidney injuryPrimary malignancySecondary inflammationTubular damageTubulointerstitial nephritisBronchogenic carcinomaInfiltrative lesionsLymphoproliferative disordersCell carcinomaMetastatic spreadBreast cancerPrimary involvementNormal kidneySolid cancersCell disordersTubular cellsTubular lumenBlood cellsDiseaseCharacterization of temporospatial distribution of renal tubular casts by nephron tracking after ischemia-reperfusion injury
Shin NS, Marlier A, Xu L, Lam T, Cantley LG, Guo JK. Characterization of temporospatial distribution of renal tubular casts by nephron tracking after ischemia-reperfusion injury. American Journal Of Physiology. Renal Physiology 2022, 322: f322-f334. PMID: 35100823, PMCID: PMC8897010, DOI: 10.1152/ajprenal.00284.2021.Peer-Reviewed Original ResearchConceptsIschemia-reperfusion injuryCast formationGlomerular filtration rateTubular cast formationUrine 24 hDetached epithelial cellsDead cell debrisRenal recoveryRenal functionFiltration rateS3 tubulesTubular castsTubular cellsTubular nucleiKidney sectionsOuter medullaTrypsin levelsEntire nephronRenal tubular castsFuture interventionsInjurySelective lossTubule segmentsEpithelial cellsKidney
2021
Expression of human CD47 in pig glomeruli prevents proteinuria and prolongs graft survival following pig‐to‐baboon xenotransplantation
Takeuchi K, Ariyoshi Y, Shimizu A, Okumura Y, Cara‐Fuentes G, Garcia G, Pomposelli T, Watanabe H, Boyd L, Ekanayake‐Alper D, Amarnath D, Sykes M, Sachs D, Johnson R, Yamada K. Expression of human CD47 in pig glomeruli prevents proteinuria and prolongs graft survival following pig‐to‐baboon xenotransplantation. Xenotransplantation 2021, 28: e12708. PMID: 34418164, PMCID: PMC8957703, DOI: 10.1111/xen.12708.Peer-Reviewed Original ResearchConceptsDevelopment of proteinuriaKidney graftsRenal tubular cellsGlomerular cellsTubular cellsNephrotic syndromeHuman CD47Transgene expressionPig-to-baboon xenotransplantationBone marrow transplantationDestructive inflammatory responseUpregulation of CD80Pig-to-baboonSMPDL-3bPigsMarrow transplantationGalT-KOGraft survivalProlonged survivalAntibody administrationThymic graftsHCD47Kidney xenotransplantationVascularized thymic graftsGroup BTubular Cell Dropout in Preimplantation Deceased Donor Biopsies as a Predictor of Delayed Graft Function
Avigan ZM, Singh N, Kliegel JA, Weiss M, Moeckel GW, Cantley LG. Tubular Cell Dropout in Preimplantation Deceased Donor Biopsies as a Predictor of Delayed Graft Function. Transplantation Direct 2021, 7: e716. PMID: 34476295, PMCID: PMC8384397, DOI: 10.1097/txd.0000000000001168.Peer-Reviewed Original ResearchDeceased donor kidney transplantDonor biopsiesGraft functionTubular injuryTubular cellsDelayed graft functionAcute tubular injuryDonor kidney transplantsConventional histopathologic evaluationPotential therapeutic interventionsMass cytometry analysisTubular cell lossDGF riskGraft outcomeTransplant recipientsKidney transplantPharmacologic therapyDeceased donorsMacrophage infiltrationHistopathologic evaluationLiving donorsDonor factorsCold ischemiaHistopathologic analysisCell dropout
2019
Tubular GM-CSF Promotes Late MCP-1/CCR2-Mediated Fibrosis and Inflammation after Ischemia/Reperfusion Injury
Xu L, Sharkey D, Cantley LG. Tubular GM-CSF Promotes Late MCP-1/CCR2-Mediated Fibrosis and Inflammation after Ischemia/Reperfusion Injury. Journal Of The American Society Of Nephrology 2019, 30: 1825-1840. PMID: 31315923, PMCID: PMC6779361, DOI: 10.1681/asn.2019010068.Peer-Reviewed Original ResearchConceptsIschemia/reperfusion injuryWild-type miceTubular cellsTubular injuryReperfusion injuryImmune cellsKidney ischemia/reperfusion injuryUnilateral ischemia/reperfusion injuryMCP-1/CCR2Monocyte chemoattractant protein-1Initial kidney damageInjured tubular cellsKidney 14 daysKidney injury markersProgressive interstitial fibrosisProfibrotic growth factorsChemoattractant protein-1MCP-1 receptorGranulocyte-macrophage colony-stimulating factorRenal tubular cellsNumber of macrophagesTime of repairColony-stimulating factorCoculture of macrophagesMacrophages persist
2018
33 Acute Interstitial Nephritis
Brewster U, Luciano R. 33 Acute Interstitial Nephritis. 2018, 320-325. DOI: 10.1016/b978-0-323-47794-9.00033-0.Peer-Reviewed Original ResearchAcute interstitial nephritisInterstitial nephritisCellular interstitial infiltratesForm of AKITriad of feverSetting of infectionUrine of patientsOccasional plasma cellsRenal tubular cellsKidney injuryMedication exposureSterile pyuriaCulprit medicationKidney biopsyMild proteinuriaInterstitial infiltratesSystemic diseaseAutoimmune diseasesDefinitive diagnosisCommon causePlasma cellsImmune responseUrine sedimentTubular cellsRapid treatment
2017
MIF-2/D-DT enhances proximal tubular cell regeneration through SLPI- and ATF4-dependent mechanisms
Ochi A, Chen D, Schulte W, Leng L, Moeckel N, Piecychna M, Averdunk L, Stoppe C, Bucala R, Moeckel G. MIF-2/D-DT enhances proximal tubular cell regeneration through SLPI- and ATF4-dependent mechanisms. American Journal Of Physiology. Renal Physiology 2017, 313: f767-f780. PMID: 28539339, PMCID: PMC6148305, DOI: 10.1152/ajprenal.00683.2016.Peer-Reviewed Original ResearchMeSH KeywordsActivating Transcription Factor 4Acute Kidney InjuryAnimalsAntigens, Differentiation, B-LymphocyteApoptosisAutophagyCell HypoxiaCell LineCell ProliferationCyclin D1Disease Models, AnimalEukaryotic Initiation Factor-2FemaleGenetic Predisposition to DiseaseHistocompatibility Antigens Class IIIntramolecular OxidoreductasesKidney Tubules, ProximalMacrophage Migration-Inhibitory FactorsMaleMice, Inbred C57BLMice, KnockoutPhenotypeRegenerationReperfusion InjurySecretory Leukocyte Peptidase InhibitorSignal TransductionTime FactorsTransfectionConceptsMacrophage migration inhibitory factorSecretory leukocyte proteinase inhibitorTubular cell regenerationProximal tubular cellsD-DTCell regenerationTubular cellsIschemic acute kidney injuryIschemia-reperfusion injury modelWild-type control miceMouse proximal tubular cellsAcute kidney injuryIschemia-reperfusion injuryRenal proximal tubular cellsMigration inhibitory factorIntegrated stress responseATF4-dependent mechanismCyclin D1 expressionEukaryotic initiation factorKidney injuryTubular injuryControl miceChemokine receptorsInjury modelInflammatory context
2016
FAT1 mutations cause a glomerulotubular nephropathy
Gee HY, Sadowski CE, Aggarwal PK, Porath JD, Yakulov TA, Schueler M, Lovric S, Ashraf S, Braun DA, Halbritter J, Fang H, Airik R, Vega-Warner V, Cho KJ, Chan TA, Morris LG, ffrench-Constant C, Allen N, McNeill H, Büscher R, Kyrieleis H, Wallot M, Gaspert A, Kistler T, Milford DV, Saleem MA, Keng WT, Alexander SI, Valentini RP, Licht C, Teh JC, Bogdanovic R, Koziell A, Bierzynska A, Soliman NA, Otto EA, Lifton RP, Holzman LB, Sibinga NE, Walz G, Tufro A, Hildebrandt F. FAT1 mutations cause a glomerulotubular nephropathy. Nature Communications 2016, 7: 10822. PMID: 26905694, PMCID: PMC4770090, DOI: 10.1038/ncomms10822.Peer-Reviewed Original ResearchConceptsSteroid-resistant nephrotic syndromeChronic kidney diseaseKnockdown of Fat1Podocyte foot process effacementTubular cell functionRenal tubular cellsFoot process effacementNephrotic syndromeNeurological involvementKidney diseaseFAT1 mutationsDisease entityPodocyte-specific deletionTubular cellsTubular ectasiaProcess effacementCell functionDecreased migrationRac1/Cdc42PathogenesisFAT1Barrier developmentKnockdownRecessive mutationsHaematuria
2014
GM-CSF Promotes Macrophage Alternative Activation after Renal Ischemia/Reperfusion Injury
Huen SC, Huynh L, Marlier A, Lee Y, Moeckel GW, Cantley LG. GM-CSF Promotes Macrophage Alternative Activation after Renal Ischemia/Reperfusion Injury. Journal Of The American Society Of Nephrology 2014, 26: 1334-1345. PMID: 25388222, PMCID: PMC4446881, DOI: 10.1681/asn.2014060612.Peer-Reviewed Original ResearchMeSH KeywordsAcute Kidney InjuryAnalysis of VarianceAnimalsBlotting, WesternCell ProliferationCells, CulturedDisease Models, AnimalGene Expression RegulationGranulocyte-Macrophage Colony-Stimulating FactorImmunohistochemistryKidney Tubules, ProximalMacrophage ActivationMaleMiceMice, Inbred C57BLMultivariate AnalysisPhenotypeRandom AllocationReal-Time Polymerase Chain ReactionReperfusion InjurySignal TransductionUp-RegulationConceptsIschemia/reperfusion injuryMacrophage alternative activationBone marrow-derived macrophagesAlternative activationMarrow-derived macrophagesTubular cellsGM-CSFReperfusion injuryReparative phenotypeTubular proliferationKidney ischemia/reperfusion injuryRenal ischemia/reperfusion injuryMouse proximal tubule cellsInitial kidney damageRepair phaseProximal tubule cellsTubular factorsIschemic injuryKidney damageProinflammatory macrophagesRenal repairMacrophage activationTubule cellsPharmacologic inhibitionMacrophagesBile Acid Nephropathy in a Bodybuilder Abusing an Anabolic Androgenic Steroid
Luciano RL, Castano E, Moeckel G, Perazella MA. Bile Acid Nephropathy in a Bodybuilder Abusing an Anabolic Androgenic Steroid. American Journal Of Kidney Diseases 2014, 64: 473-476. PMID: 24953892, DOI: 10.1053/j.ajkd.2014.05.010.Peer-Reviewed Case Reports and Technical NotesConceptsAcute kidney injurySevere cholestatic liver diseaseCholestatic liver diseaseLiver diseaseAcute tubular injury/necrosisCases of AKIEnd-stage liver diseaseBile acid injurySevere obstructive jaundiceAcute tubular injuryAnabolic androgenic steroidsAnabolic-androgenic steroid useCholemic nephrosisHepatorenal syndromeKidney injuryTubular injuryObstructive jaundiceHemodynamic changesTubular toxicitySteroid useAcid injuryHepatic diseaseTubular cellsHeterogeneous lesionsNephropathyRenalase Prevents AKI Independent of Amine Oxidase Activity
Wang L, Velazquez H, Moeckel G, Chang J, Ham A, Lee HT, Safirstein R, Desir GV. Renalase Prevents AKI Independent of Amine Oxidase Activity. Journal Of The American Society Of Nephrology 2014, 25: 1226-1235. PMID: 24511138, PMCID: PMC4033373, DOI: 10.1681/asn.2013060665.Peer-Reviewed Original ResearchConceptsIschemic injuryCatecholamine levelsRecombinant renalaseAmine oxidase activityHuman proximal tubular cellsCisplatin-induced AKITreatment of AKIWild-type miceHK-2 cellsProximal tubular cellsOxidase activityKidney injuryRenal injuryC-Jun N-terminal kinaseExtracellular signal-regulated kinaseP38 mitogen-activated protein kinaseToxic injuryRenalase proteinTubular cellsSignal-regulated kinaseIntracellular signaling cascadesRenalaseInjuryMitogen-activated protein kinaseN-terminal kinase
2013
Chapter 65 The Hormonal Regulation of Calcium Metabolism
Tebben P, Kumar R. Chapter 65 The Hormonal Regulation of Calcium Metabolism. 2013, 2249-2272. DOI: 10.1016/b978-0-12-381462-3.00065-3.ChaptersRegulation of calcium metabolismParathyroid hormoneCalcium metabolismExtracellular fluid calcium concentrationCalcium homeostasisControl of calcium homeostasisHormonal regulation of calcium metabolismCellular signalingEnzyme functionBiological processesRenal tubular cellsPathophysiology of diseaseHormonal regulationSevere calcium deficiencyValvular calcificationMuscular contractilityNormal rangeMal seizuresTubular cellsCalcium concentrationNeuromuscular transmissionHormoneEctopic sitesBlood coagulationHomeostasis
2011
Increased Tubular Proliferation as an Adaptive Response to Glomerular Albuminuria
Guo JK, Marlier A, Shi H, Shan A, Ardito TA, Du ZP, Kashgarian M, Krause DS, Biemesderfer D, Cantley LG. Increased Tubular Proliferation as an Adaptive Response to Glomerular Albuminuria. Journal Of The American Society Of Nephrology 2011, 23: 429-437. PMID: 22193389, PMCID: PMC3294312, DOI: 10.1681/asn.2011040396.Peer-Reviewed Original ResearchMeSH KeywordsAlbuminuriaAnimalsAxl Receptor Tyrosine KinaseCell ProliferationDisease Models, AnimalFemaleHeparin-binding EGF-like Growth FactorIntegrasesIntercellular Signaling Peptides and ProteinsIntracellular Signaling Peptides and ProteinsKidney GlomerulusKidney Tubules, ProximalMaleMembrane ProteinsMiceMice, TransgenicPodocytesProteinuriaProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesConceptsGlomerular proteinuriaTubular injuryTubular proliferationStructural glomerular injuryProteinuric renal diseaseOnset of albuminuriaRenal tubular atrophyDiphtheria toxin receptorRenal tubular cellsProximal tubule cellsGlomerular albuminuriaRenal failureSystemic inflammationTubular damageProgressive glomerulosclerosisRenal diseaseTubular atrophyGlomerular injuryRenal responsePodocyte lossProliferative responseTubular cellsAnimal modelsProteinuriaReceptor AxlMacrophages Promote Cyst Growth in Polycystic Kidney Disease
Karihaloo A, Koraishy F, Huen SC, Lee Y, Merrick D, Caplan MJ, Somlo S, Cantley LG. Macrophages Promote Cyst Growth in Polycystic Kidney Disease. Journal Of The American Society Of Nephrology 2011, 22: 1809-1814. PMID: 21921140, PMCID: PMC3187181, DOI: 10.1681/asn.2011010084.Peer-Reviewed Original ResearchConceptsPolycystic kidney diseaseCyst-lining cellsKidney diseaseCyst growthPkd1-deficient cellsContribution of inflammationMacrophage-depleted miceVehicle-treated controlsPostnatal day 10Renal functionInflammatory componentIschemic injuryOrthologous modelCre miceCystic areasLiposomal clodronateCyst progressionRenal parenchymaCystic indexTubular cellsDay 10Therapeutic potentialDay 24Macrophage migrationMacrophages
2008
Erythropoietin expands a stromal cell population that can mediate renoprotection
Bi B, Guo J, Marlier A, Lin SR, Cantley LG. Erythropoietin expands a stromal cell population that can mediate renoprotection. American Journal Of Physiology. Renal Physiology 2008, 295: f1017-f1022. PMID: 18653480, PMCID: PMC2576137, DOI: 10.1152/ajprenal.90218.2008.Peer-Reviewed Original ResearchConceptsAdministration of EPOMarrow stromal cellsTubular epithelial cellsRenoprotective effectsTubular cellsCisplatin-treated miceEpithelial cellsEndothelial progenitor cellsSecretion of factorsStromal cell populationsDeprivation-induced cell deathRenal functionTubular injuryCisplatin administrationPeripheral circulationIntraperitoneal injectionSerum deprivation-induced cell deathToxic injuryBone marrowStromal cellsVivo expansionInjuryProgenitor cellsAdministrationEPO receptor
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