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 castsGenetic deficiency or pharmacological inhibition of cGAS–STING signalling suppresses kidney inflammation and fibrosis
Jiao B, An C, Du H, Tran M, Yang D, Zhao Y, Wang P, Hu Z, Zhou D, Wang Y. Genetic deficiency or pharmacological inhibition of cGAS–STING signalling suppresses kidney inflammation and fibrosis. British Journal Of Pharmacology 2025, 182: 1741-1762. PMID: 39833988, DOI: 10.1111/bph.17412.Peer-Reviewed Original ResearchChronic kidney diseaseMacrophage proinflammatory activationDevelopment of renal fibrosisObstructive injuryCGAS-STING signalingProinflammatory activityCGAS-STINGRenal inflammationRenal fibrosisPharmacological inhibitionMyofibroblast formationDamaged tubular epithelial cellsCyclic GMP-AMP synthase (cGAS)-stimulatorBone marrow-derived macrophagesAttenuated kidney fibrosisMarrow-derived macrophagesCGAS-STING signaling pathwayTubular epithelial cellsSignaling in vitroCell-derived DNAPreclinical modelsTubular atrophySTING deficiencyInhibition of cGASKidney inflammation
2024
Glucosamine mitigates ischemia-reperfusion-induced acute kidney injury through anti-inflammatory mechanisms
Zhang G, Jin S, Fan X, Qi J, Liu J, Yin S, Cao Y, Du Y, Dong X, Wang Z, Tan X, Yan S. Glucosamine mitigates ischemia-reperfusion-induced acute kidney injury through anti-inflammatory mechanisms. Frontiers In Materials 2024, 11: 1438610. DOI: 10.3389/fmats.2024.1438610.Peer-Reviewed Original ResearchAcute kidney injuryTubular epithelial cellsKidney injuryI/R injuryRenal tissueEpithelial cellsInflammatory responseRenal ischemia-reperfusion (I/R) injuryIschemia-reperfusion-induced acute kidney injuryI/R-induced acute kidney injuryEndoplasmic reticulumIschemia-reperfusion (I/R) injuryProximal tubular epithelial cellsMarkers of oxidative stressEfficacy of glucosaminePotential therapeutic efficacyProximal convoluted tubular epithelial cellsRenal interstitial fibrosisI/R injury modelAnti-inflammatory actionMitigate ER stressAnti-inflammatory mechanismsAssessed in vitroOxidative stress levelsReduced oxidative stress levelsUromodulin and progression of IgA nephropathy
Chen Z, Xu L, Du W, Ouyang Y, Gu X, Fang Z, Yu X, Li J, Xie L, Jin Y, Ma J, Wang Z, Pan X, Zhang W, Ren H, Wang W, Chen X, Zhou X, Zhang H, Chen N, Xie J. Uromodulin and progression of IgA nephropathy. Clinical Kidney Journal 2024, 17: sfae209. PMID: 39145144, PMCID: PMC11322676, DOI: 10.1093/ckj/sfae209.Peer-Reviewed Original ResearchEnd-stage renal diseaseSingle-nucleotide polymorphismsIgAN patientsAllele-specific enhancer activityKidney functionAssociated with renal function deteriorationGenome-wide association studiesFunction of genetic variationBiopsy-proven IgAN patientsProgression of IgA nephropathyRenal pathological dataEnd-stage renal disease patientsRenal function deteriorationTubular epithelial cellsEnhanced activityRenal tubular epitheliumIgAN progressionUromodulin expressionNo significant differenceGenetic variationRuijin HospitalUromodulin levelsPathological dataIgA nephropathyRenal disease
2023
VPA improves ferroptosis in tubular epithelial cells after cisplatin-induced acute kidney injury
Li Y, Li K, Zhao W, Wang H, Xue X, Chen X, Li W, Xu P, Wang K, Liu P, Tian X, Fu R. VPA improves ferroptosis in tubular epithelial cells after cisplatin-induced acute kidney injury. Frontiers In Pharmacology 2023, 14: 1147772. PMID: 37153759, PMCID: PMC10155836, DOI: 10.3389/fphar.2023.1147772.Peer-Reviewed Original ResearchCisplatin-induced acute kidney injuryAcute kidney injuryAcyl-CoA synthetase long-chain family member 4Valproic acidKidney injuryTubular epithelial cellsGlutathione peroxidase 4Renal injuryDownregulation of GPX4Cisplatin-induced AKI miceCisplatin-induced renal injuryFer-1 treatmentEpithelial cellsBlood urea nitrogenCell deathFamily member 4AKI miceSerum creatinineAntiepileptic drugsHistone deacetylase 1Protective effectUrea nitrogenViable treatmentTissue damageCisplatin treatment
2021
Interdependent Regulation of Polycystin Expression Influences Starvation-Induced Autophagy and Cell Death
Decuypere JP, Van Giel D, Janssens P, Dong K, Somlo S, Cai Y, Mekahli D, Vennekens R. Interdependent Regulation of Polycystin Expression Influences Starvation-Induced Autophagy and Cell Death. International Journal Of Molecular Sciences 2021, 22: 13511. PMID: 34948309, PMCID: PMC8706473, DOI: 10.3390/ijms222413511.Peer-Reviewed Original ResearchConceptsProximal tubular epithelial cellsAutosomal dominant polycystic kidney diseaseEarly-stage ADPKD patientsCell deathPC2 expressionDominant polycystic kidney diseaseTubular epithelial cellsRenal cell survivalPolycystin-1Polycystic kidney diseaseCell survivalPolycystin-2Basal autophagyAutophagic cell survivalCell death resistanceADPKD progressionKidney diseaseADPKD patientsLess cell deathPC1 levelsChronic starvationHealthy individualsDuct cellsEpithelial cellsDeathCoronavirus Disease (COVID)-19 and Diabetic Kidney Disease
Srivastava SP, Srivastava R, Chand S, Goodwin JE. Coronavirus Disease (COVID)-19 and Diabetic Kidney Disease. Pharmaceuticals 2021, 14: 751. PMID: 34451848, PMCID: PMC8398861, DOI: 10.3390/ph14080751.Peer-Reviewed Original ResearchCell typesDiabetic kidney diseaseCOVID-19 patientsSuppression of AMPProtein kinase activationKidney cellsMAS1 receptorCellular homeostasisKidney diseaseKinase activationCell homeostasisAcute respiratory syndrome coronavirus 2 infectionSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infectionTransferase 4Diabetic COVID-19 patientsSyndrome coronavirus 2 infectionCoronavirus 2 infectionAMPK levelsDPP-4 levelsCOVID-19 severityCOVID-19-associated cytokine stormTubular epithelial cellsMesenchymal activationOrgan fibrosisNovel drug therapiesFC 008INTERDEPENDENT REGULATION OF POLYCYSTIN EXPRESSION INFLUENCES STARVATION-INDUCED AUTOPHAGY AND CELL DEATH
Decuypere J, Van Giel D, Janssens P, Dong K, Somlo S, Cai Y, Mekahli D, Vennekens R. FC 008INTERDEPENDENT REGULATION OF POLYCYSTIN EXPRESSION INFLUENCES STARVATION-INDUCED AUTOPHAGY AND CELL DEATH. Nephrology Dialysis Transplantation 2021, 36: gfab125.001. DOI: 10.1093/ndt/gfab125.001.Peer-Reviewed Original ResearchAutosomal dominant polycystic kidney diseaseEarly-stage ADPKD patientsProximal tubular epithelial cellsProteins polycystin-1Renal stressADPKD patientsEarly-stage autosomal dominant polycystic kidney diseasePC1 levelsCell deathCyst formationTruncating PKD1 mutationsSevere disease progressionAutophagy upregulationDominant polycystic kidney diseaseTubular epithelial cellsRenal cell survivalPolycystic kidney diseasePolycystin-2Cell survivalCell death resistanceKidney diseaseDisease progressionGFP-LC3 punctaeSiRNA-mediated knockdownChronic starvationLoss of endothelial glucocorticoid receptor accelerates diabetic nephropathy
Srivastava SP, Zhou H, Setia O, Liu B, Kanasaki K, Koya D, Dardik A, Fernandez-Hernando C, Goodwin J. Loss of endothelial glucocorticoid receptor accelerates diabetic nephropathy. Nature Communications 2021, 12: 2368. PMID: 33888696, PMCID: PMC8062600, DOI: 10.1038/s41467-021-22617-y.Peer-Reviewed Original ResearchMeSH KeywordsAdrenalectomyAnimalsDiabetes Mellitus, ExperimentalDiabetic NephropathiesEndothelial CellsEndotheliumEpithelial-Mesenchymal TransitionFatty AcidsFibrosisGlucocorticoidsHumansHypercholesterolemiaInterleukin-6Kidney TubulesMaleMiceMice, Knockout, ApoEOxidation-ReductionReceptors, GlucocorticoidStreptozocinWnt Signaling PathwayConceptsEndothelial glucocorticoid receptorGlucocorticoid receptorEndothelial cell homeostasisDiabetic miceRenal fibrosisEndothelial cellsMesenchymal transitionSevere renal fibrosisTubular epithelial cellsCell homeostasisFatty acid oxidationDiabetic controlDiabetic nephropathyAntifibrotic moleculesIL-6Kidney fibrosisMesenchymal activationRegulation of diseaseOrgan fibrosisAberrant cytokineFibrogenic phenotypeFibrosisMiceEpithelial cellsDefective regulationEndothelial SIRT3 regulates myofibroblast metabolic shifts in diabetic kidneys
Srivastava SP, Li J, Takagaki Y, Kitada M, Goodwin JE, Kanasaki K, Koya D. Endothelial SIRT3 regulates myofibroblast metabolic shifts in diabetic kidneys. IScience 2021, 24: 102390. PMID: 33981977, PMCID: PMC8086030, DOI: 10.1016/j.isci.2021.102390.Peer-Reviewed Original ResearchDiabetic kidney fibrosisDiabetic kidneyEndothelial cellsKidney fibrosisDefective metabolismRenal tubular epithelial cellsTubular epithelial cellsKidney functionDiabetic miceFibrogenic pathwaysFibrogenic processDisease processLoss of functionMesenchymal transitionKidneyMouse strainsEpithelial cellsGain of functionSIRT3Metabolic reprogrammingMesenchymal transformationFibrosisSIRT3 geneMetabolismCells
2020
Loss of IL-27Rα Results in Enhanced Tubulointerstitial Fibrosis Associated with Elevated Th17 Responses.
Coppock GM, Aronson LR, Park J, Qiu C, Park J, DeLong JH, Radaelli E, Suszták K, Hunter CA. Loss of IL-27Rα Results in Enhanced Tubulointerstitial Fibrosis Associated with Elevated Th17 Responses. The Journal Of Immunology 2020, 205: 377-386. PMID: 32522836, PMCID: PMC7368461, DOI: 10.4049/jimmunol.1901463.Peer-Reviewed Original ResearchConceptsChronic kidney diseaseUnilateral ureteral obstructionIL-17AIL-27RαIL-27Ureteral obstructionKidney diseaseIL-27 actsImmune cell infiltratesCytokine IL-27Day of surgeryImmune-mediated pathologyTubular epithelial cellsDegree of injuryFibrosis AssociatedKidney injuryTh17 cellsTh17 responsesCell infiltrateSerum levelsInflammatory cascadeRenal fibrosisIL-17RAImmune cellsChemokine mRNASignaling through tumor necrosis receptor 2 induces stem cell marker in CD133+ regenerating tubular epithelial cells in acute cell-mediated rejection of human renal allografts
Bradley JR, Wang J, Bardsley V, Broecker V, Thiru S, Pober JS, Al-Lamki R. Signaling through tumor necrosis receptor 2 induces stem cell marker in CD133+ regenerating tubular epithelial cells in acute cell-mediated rejection of human renal allografts. American Journal Of Transplantation 2020, 20: 2380-2391. PMID: 32167668, DOI: 10.1111/ajt.15846.Peer-Reviewed Original Research
2019
Monoclonal Gammopathy of Renal Significance Triggered by Viral E Hepatitis
Agrawal P, Kumar V, Kumar A, Sachdeva M, Malhotra P, Nada R. Monoclonal Gammopathy of Renal Significance Triggered by Viral E Hepatitis. Indian Journal Of Nephrology 2019, 29: 50-52. PMID: 30814794, PMCID: PMC6375020, DOI: 10.4103/ijn.ijn_417_17.Peer-Reviewed Original ResearchMonoclonal gammopathy of renal significanceLight chain cast nephropathyMonoclonal gammopathyRenal significanceCast nephropathyDrug-induced interstitial nephritisAcute hepatitis E infectionBone marrow examinationAcute hepatitis EHepatitis E infectionTubular epithelial cellsProportion of casesMGRS lesionsMarrow examinationClinical suspicionProximal tubulopathyGiant cell reactionElevated creatinineKappa restrictionSerum calciumKidney biopsyB2-microglobulinRenal injuryPlasma cellsInterstitial nephritis
2018
The protective role of macrophage migration inhibitory factor in acute kidney injury after cardiac surgery
Stoppe C, Averdunk L, Goetzenich A, Soppert J, Marlier A, Kraemer S, Vieten J, Coburn M, Kowark A, Kim BS, Marx G, Rex S, Ochi A, Leng L, Moeckel G, Linkermann A, El Bounkari O, Zarbock A, Bernhagen J, Djudjaj S, Bucala R, Boor P. The protective role of macrophage migration inhibitory factor in acute kidney injury after cardiac surgery. Science Translational Medicine 2018, 10 PMID: 29769287, DOI: 10.1126/scitranslmed.aan4886.Peer-Reviewed Original ResearchMeSH KeywordsAcute Kidney InjuryAnimalsAntigens, Differentiation, B-LymphocyteAntioxidantsCardiac Surgical ProceduresCell DeathHistocompatibility Antigens Class IIHumansIncidenceInflammationKidneyLipid PeroxidationLipocalin-2Macrophage Migration-Inhibitory FactorsMice, Inbred C57BLOxidative StressProtective AgentsProtein DomainsRecombinant ProteinsReperfusion InjuryRhabdomyolysisConceptsMacrophage migration inhibitory factorAcute kidney injuryRecombinant macrophage migration inhibitory factorIschemia-reperfusion injuryCardiac surgeryMigration inhibitory factorTubular epithelial cellsKidney injuryHigher macrophage migration inhibitory factorIncidence of AKIPathogenesis of AKIUrinary Macrophage Migration Inhibitory FactorExperimental acute kidney injuryExperimental ischemia-reperfusion injuryInhibitory factorMyocardial ischemia-reperfusion injuryOxidative stressMIF serum concentrationsCardiac surgery patientsRenal tubular epithelial cellsConventional cardiac surgeryEpithelial cellsHours of reperfusionSetting of hypoxiaTubular cell injuryBlue-green discoloration of urine and false nephrotic range proteinuria at dipstick urinalysis
Poloni J, de Moraes Sassi M, de Oliveira T, Rotta L, Perazella M. Blue-green discoloration of urine and false nephrotic range proteinuria at dipstick urinalysis. Clinica Chimica Acta 2018, 482: 74-77. PMID: 29608875, DOI: 10.1016/j.cca.2018.03.036.Peer-Reviewed Original ResearchConceptsHigh-power fieldCells/high power fieldLeukocytes/high-power fieldBlue-green discolorationUrine samplesRenal tubular epithelial cellsNephrotic range proteinuriaUrinary tract infectionYear old womanUrine protein concentrationTubular epithelial cellsAlbumin 3Range proteinuriaTract infectionsCellular castsDipstick urinalysisEmergency departmentUrine sedimentBilirubin 2Epithelial cellsPower fieldUrinalysisMethylthioninium chloride
2017
Kidney Injury and Repair Biomarkers in Marathon Runners
Mansour SG, Verma G, Pata RW, Martin TG, Perazella MA, Parikh CR. Kidney Injury and Repair Biomarkers in Marathon Runners. American Journal Of Kidney Diseases 2017, 70: 252-261. PMID: 28363731, PMCID: PMC5526736, DOI: 10.1053/j.ajkd.2017.01.045.Peer-Reviewed Original ResearchConceptsCreatinine levelsDay 0Kidney injuryTubular injuryUrine albuminSerum creatinineKidney functionUrine biomarkersBiomarker levelsSerum creatine kinase levelsMarathon runnersAKI Network criteriaAKI stage 1Stage 1 AKISerum creatinine levelsRenal tubular epithelial cellsLimited clinical dataCreatine kinase levelsTubular epithelial cellsDL increaseMean ageMicroscopy scoreGranular castsClinical dataObservational study
2016
The lymphotoxin β receptor is a potential therapeutic target in renal inflammation
Seleznik G, Seeger H, Bauer J, Fu K, Czerkowicz J, Papandile A, Poreci U, Rabah D, Ranger A, Cohen CD, Lindenmeyer M, Chen J, Edenhofer I, Anders HJ, Lech M, Wüthrich RP, Ruddle NH, Moeller MJ, Kozakowski N, Regele H, Browning JL, Heikenwalder M, Segerer S. The lymphotoxin β receptor is a potential therapeutic target in renal inflammation. Kidney International 2016, 89: 113-126. PMID: 26398497, DOI: 10.1038/ki.2015.280.Peer-Reviewed Original ResearchMeSH KeywordsAdultAnimalsCell LineChemokinesDisease Models, AnimalEpithelial CellsFemaleGlomerulonephritis, IGAHumansImmunoglobulinsKidney GlomerulusKidney TubulesLigandsLupus NephritisLymphocytesLymphotoxin beta ReceptorLymphotoxin-alphaLymphotoxin-betaMaleMesangial CellsMiceMiddle AgedRNA, MessengerSignal TransductionTranscriptomeConceptsTubular epithelial cellsParietal epithelial cellsEpithelial cellsRenal injuryLTβR signalingTherapeutic targetGlomerular immune complex depositionLymphotoxin β receptor (LTβR) signalingImproved renal functionSerum autoantibody titersHuman tubular epithelial cellsImmune complex depositionMurine lupus modelsProgressive kidney diseaseSuitable therapeutic targetPreclinical mouse modelsDifferent renal compartmentsPotential therapeutic targetΒ Receptor SignalingLymphotoxin β receptorAutoantibody titersRenal inflammationLupus modelsRenal functionRenal biopsy
2015
Drug-induced acute interstitial nephritis: pathology, pathogenesis, and treatment.
Krishnan N, Perazella MA. Drug-induced acute interstitial nephritis: pathology, pathogenesis, and treatment. Iranian Journal Of Kidney Diseases 2015, 9: 3-13. PMID: 25599729.BooksConceptsDrug-induced acute interstitial nephritisCell-mediated immune injuryLess chronic kidney diseaseAcute interstitial nephritisHallmark pathologic featureIncomplete renal recoveryInterstitial dendritic cellsNeo-antigen formationPredominance of CD4Acute kidney injurySerum creatinine levelsChronic kidney diseaseMainstay of treatmentRenal tubular epithelial cellsUse of steroidsDuration of injuryTubular epithelial cellsRenal recoveryChronic dialysisKidney injuryCreatinine levelsImmunologic injuryInterstitial inflammationDendritic cellsImmune injury
2014
Quantification and localization of M2 macrophages in human kidneys with acute tubular injury
Palmer MB, Vichot AA, Cantley LG, Moeckel GW. Quantification and localization of M2 macrophages in human kidneys with acute tubular injury. International Journal Of Nephrology And Renovascular Disease 2014, 7: 415-419. PMID: 25404860, PMCID: PMC4230184, DOI: 10.2147/ijnrd.s66936.Peer-Reviewed Original ResearchAcute tubular injuryMinimal change diseaseM2 macrophagesTubular epithelial cellsTubular injuryMacrophage populationsEpithelial cellsBiopsy-proven diagnosisUltra-structural examinationProximal tubule cellsTubular basement membraneBasement membraneHuman kidney sectionsHuman kidney tissueHLA-DRChange diseaseAbove diagnosisInterstitial macrophagesM1 macrophagesM2 phenotypeInterstitial macrophage populationKidney sectionsKidney tissuePatientsTubule cells
2013
Cytomegalovirus Glomerulopathy and Cytomegalovirus Interstitial Nephritis on Sequential Transplant Kidney Biopsies
Vichot AA, Formica RN, Moeckel GW. Cytomegalovirus Glomerulopathy and Cytomegalovirus Interstitial Nephritis on Sequential Transplant Kidney Biopsies. American Journal Of Kidney Diseases 2013, 63: 536-539. PMID: 24568687, PMCID: PMC7210789, DOI: 10.1053/j.ajkd.2013.08.021.Peer-Reviewed Original ResearchConceptsSecond biopsy specimenBiopsy specimenCMV infectionInterstitial nephritisKidney biopsyKidney transplant biopsy specimensEndothelial cellsCMV-negative patientsCMV-positive cellsCMV-positive donorsFirst biopsy specimenKidney transplant graftsSequential kidney biopsiesTransplant biopsy specimensTransplant kidney biopsiesGlomerular capillary endothelial cellsTubular epithelial cellsGlomerular capillary loopsGlomerular capillary luminaCapillary endothelial cellsCytoplasmic viral particlesKidney transplantTubular injuryLymphoplasmacytic infiltrateTransplant grafts
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