2024
Characteristics of renal pathology and coagulation function in IgA nephropathy and IgA vasculitis associated nephritis
Wang Y, Wang H, Ma X, Zhu Z, Tian X, Fu R, Jia L. Characteristics of renal pathology and coagulation function in IgA nephropathy and IgA vasculitis associated nephritis. BMC Nephrology 2024, 25: 35. PMID: 38273279, PMCID: PMC10811929, DOI: 10.1186/s12882-024-03465-6.Peer-Reviewed Original ResearchConceptsIgAN patientsFibrinogen degradation productsIgA nephropathyIgAVN patientsLevels of plasma D-dimerLevels of serum creatininePartial remission rateSevere coagulation abnormalitiesPlasma D-dimerPoor renal functionChronic kidney injuryRemission ratePathological resultsSerum creatinineAbdominal symptomsRenal functionCoagulation abnormalitiesDeposition of fibrinogenKidney biopsyD-dimerKidney injuryCoagulation functionIgAVNIgAN groupMethodsA totalEditorial: Association between diabetic nephropathy and diabetic retinopathy or non-diabetic nephropathy
Chen H, Tian X, Yu X. Editorial: Association between diabetic nephropathy and diabetic retinopathy or non-diabetic nephropathy. Frontiers In Endocrinology 2024, 15: 1359011. PMID: 38332890, PMCID: PMC10852059, DOI: 10.3389/fendo.2024.1359011.Commentaries, Editorials and LettersUnderstanding the podocyte immune responses in proteinuric kidney diseases: from pathogenesis to therapy
Jiang H, Shen Z, Zhuang J, Lu C, Qu Y, Xu C, Yang S, Tian X. Understanding the podocyte immune responses in proteinuric kidney diseases: from pathogenesis to therapy. Frontiers In Immunology 2024, 14: 1335936. PMID: 38288116, PMCID: PMC10822972, DOI: 10.3389/fimmu.2023.1335936.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsChronic kidney diseaseGlomerular filtration barrierProteinuric glomerular diseasesKidney diseaseGlomerular diseaseImmune responseFiltration barrierTherapeutic targetCell-like characteristicsFocal segmental glomerulosclerosisProteinuric kidney diseaseTargets of immune responsesDamage to podocytesLupus nephritisPotential therapeutic targetGlomerular basement membraneImmune injuryGlomerular injuryMembranous nephropathyFenestrated endothelial cellsKidney functionSegmental glomerulosclerosisAdaptive immunityEpithelial cellsPathogenic mechanisms
2023
Profilin1 is required to prevent mitotic catastrophe in murine and human glomerular diseases
Tian X, Pedigo C, Li K, Ma X, Bunda P, Pell J, Lek A, Gu J, Zhang Y, Rangel P, Li W, Schwartze E, Nagata S, Lerner G, Perincheri S, Priyadarshini A, Zhao H, Lek M, Menon M, Fu R, Ishibe S. Profilin1 is required to prevent mitotic catastrophe in murine and human glomerular diseases. Journal Of Clinical Investigation 2023, 133: e171237. PMID: 37847555, PMCID: PMC10721156, DOI: 10.1172/jci171237.Peer-Reviewed Original ResearchConceptsProteinuric kidney diseaseKidney diseasePodocyte lossHuman glomerular diseasesMitotic catastrophePodocyte cell cycleSevere proteinuriaCell cycle reentryKidney failureGlomerular diseaseCell cycleKidney tissueG1/S checkpointUnsuccessful repairCyclin D1Glomerular integrityIrregular nucleiTissue-specific lossMouse podocytesPodocytesAltered expressionDiseaseCyclin B1Ribosome affinity purificationMultinucleated cellsAdvances in understanding and treating diabetic kidney disease: focus on tubulointerstitial inflammation mechanisms
Xu C, Ha X, Yang S, Tian X, Jiang H. Advances in understanding and treating diabetic kidney disease: focus on tubulointerstitial inflammation mechanisms. Frontiers In Endocrinology 2023, 14: 1232790. PMID: 37859992, PMCID: PMC10583558, DOI: 10.3389/fendo.2023.1232790.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsDiabetic kidney diseaseTubulointerstitial lesionsKidney diseaseInflammation mechanismsManagement of DKDEnd-stage kidney diseaseMineralocorticoid receptor antagonistsImmune-inflammatory mechanismsPro-inflammatory cytokinesAldosterone blockadeDKD outcomesInflammatory mechanismsSerious complicationsKidney functionGlomerular lesionsReceptor antagonistClinical trialsKidney volumeT cellsPreclinical studiesTubulointerstitial regionsLesionsTherapyDiseaseRecent studiesUnderstanding Nephrotic Syndrome Using Kidney Transcriptome Profiling and Computational Studies
Rangel P, Tian X. Understanding Nephrotic Syndrome Using Kidney Transcriptome Profiling and Computational Studies. Kidney360 2023, 4: e431-e433. PMID: 37103957, PMCID: PMC10371383, DOI: 10.34067/kid.0000000000000117.Commentaries, Editorials and Letters
2022
Coronavirus Lung Infection Impairs Host Immunity against Secondary Bacterial Infection by Promoting Lysosomal Dysfunction.
Peng X, Kim J, Gupta G, Agaronyan K, Mankowski MC, Korde A, Takyar SS, Shin HJ, Habet V, Voth S, Audia JP, Chang D, Liu X, Wang L, Cai Y, Tian X, Ishibe S, Kang MJ, Compton S, Wilen CB, Dela Cruz CS, Sharma L. Coronavirus Lung Infection Impairs Host Immunity against Secondary Bacterial Infection by Promoting Lysosomal Dysfunction. The Journal Of Immunology 2022, 209: 1314-1322. PMID: 36165196, PMCID: PMC9523490, DOI: 10.4049/jimmunol.2200198.Peer-Reviewed Original ResearchConceptsSARS-CoV-2Bacterial infectionsMouse modelCoronavirus infectionLysosomal dysfunctionMajor health care challengeLung immune cellsLung tissue damageSecondary bacterial infectionImpair host immunityIL-1β releaseHealth care challengesCell deathPyroptotic cell deathBacterial killing abilityIL-1βBacterial clearanceImmune cellsSecondary infectionHost immunityAlveolar macrophagesTissue damageΒ-coronavirusStructural cellsCare challengesEffect of pulsed intravenous methylprednisolone with alternative low-dose prednisone on high-risk IgA nephropathy: a 18-month prospective clinical trial
Li Y, Fu R, Gao J, Wang L, Duan Z, Tian L, Ge H, Ma X, Zhang Y, Li K, Xu P, Tian X, Chen Z. Effect of pulsed intravenous methylprednisolone with alternative low-dose prednisone on high-risk IgA nephropathy: a 18-month prospective clinical trial. Scientific Reports 2022, 12: 255. PMID: 34996948, PMCID: PMC8742122, DOI: 10.1038/s41598-021-03691-0.Peer-Reviewed Original ResearchMeSH KeywordsAdministration, IntravenousAdministration, OralAdultDisease ProgressionDrug TaperingDrug Therapy, CombinationFemaleGlomerulonephritis, IGAGlucocorticoidsHumansKidney Failure, ChronicMaleMethylprednisolonePrednisoneProspective StudiesProteinuriaPulse Therapy, DrugRemission InductionRisk AssessmentRisk FactorsTime FactorsTreatment OutcomeConceptsLow-dose prednisoneComplete remissionFP groupIntravenous methylprednisoloneHigh-risk IgA nephropathyOxford MEST-C scoreChinese Clinical Trial RegistryPulsed intravenous methylprednisoloneACEI/ARBClinical Trials RegistryProspective clinical trialsMEST-C scoreFavorable safety profilePercentage of CROral prednisoneTotal remissionAdult patientsNephropathy patientsPrednisone regimenCushing's syndromeMore patientsPrimary outcomeTrials RegistryClinical outcomesIgA nephropathy
2021
AMP-Kinase mediates regulation of glomerular volume and podocyte survival
Banu K, Lin Q, Basgen JM, Planoutene M, Wei C, Reghuvaran AC, Tian X, Shi H, Garzon F, Garzia A, Chun N, Cumpelik A, Santeusanio AD, Zhang W, Das B, Salem F, LI L, Ishibe S, Cantley LG, Kaufman L, Lemley KV, Ni Z, He JC, Murphy B, Menon MC. AMP-Kinase mediates regulation of glomerular volume and podocyte survival. JCI Insight 2021, 6: e150004. PMID: 34473647, PMCID: PMC8525649, DOI: 10.1172/jci.insight.150004.Peer-Reviewed Original ResearchAdenylate KinaseAdolescentAdultAgedAlbuminuriaAnimalsCell SizeCell SurvivalChildChild, PreschoolFemaleGene Knockdown TechniquesGlomerulonephritis, MembranousGlomerulosclerosis, Focal SegmentalHumansHypertrophyInfantKidney GlomerulusMaleMiceMicrofilament ProteinsMiddle AgedNephrectomyNephrosis, LipoidNephrotic SyndromePodocytesProportional Hazards ModelsProto-Oncogene Proteins c-fynYoung AdultProfibrotic mechanisms of DPP8 and DPP9 highly expressed in the proximal renal tubule epithelial cells
Zhang Y, Li K, Li Y, Zhao W, Wang L, Chen Z, Ma X, Yao T, Wang J, Dong W, Li X, Tian X, Fu R. Profibrotic mechanisms of DPP8 and DPP9 highly expressed in the proximal renal tubule epithelial cells. Pharmacological Research 2021, 169: 105630. PMID: 33932609, DOI: 10.1016/j.phrs.2021.105630.Peer-Reviewed Original ResearchMeSH KeywordsAdamantaneAnimalsBlotting, WesternCase-Control StudiesCell LineDipeptidasesDipeptidesDipeptidyl-Peptidases and Tripeptidyl-PeptidasesEpithelial-Mesenchymal TransitionFibrosisFluorescent Antibody TechniqueHumansKidney Tubules, ProximalMaleMiceMice, Inbred C57BLReal-Time Polymerase Chain ReactionRenal Insufficiency, ChronicConceptsTubulointerstitial fibrosisTubule epithelial cellsCKD patientsUUO miceHK-2 cell modelChronic kidney disease patientsTGF-β1/Smad signalingUnilateral ureteral obstruction animal modelEpithelial cellsKidney disease patientsHealthy control subjectsKidney biopsy specimensProximal tubule epithelial cellsRenal tubule epithelial cellsRenal proximal tubule epithelial cellsHK-2 cellsPotential therapeutic targetRenal inflammationTubulointerstitial injuryRenal functionUUO groupKidney functionProfibrotic mechanismsControl subjectsDisease patients
2020
The Potential Role of Regulatory B Cells in Idiopathic Membranous Nephropathy
Dong Z, Liu Z, Dai H, Liu W, Feng Z, Zhao Q, Gao Y, Liu F, Zhang N, Dong X, Zhou X, Du J, Huang G, Tian X, Liu B. The Potential Role of Regulatory B Cells in Idiopathic Membranous Nephropathy. Journal Of Immunology Research 2020, 2020: 7638365. PMID: 33426094, PMCID: PMC7772048, DOI: 10.1155/2020/7638365.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsIdiopathic membranous nephropathyRegulatory B cellsBreg cellsMembranous nephropathyImmune responseB cellsPathogenesis of IMNDifferent inflammatory environmentsFunction of BregsPathological autoimmune responsesRole of BregsCellular immune responsesHumoral immune responseIMN patientsImmunomodulatory cellsImmunosuppressive roleAutoimmune responseInterleukin-10Autoimmune diseasesImmune cellsInflammatory environmentEarly treatmentT cellsBregsImmunological phenomenaInhibiting calpain 1 and 2 in cyclin G associated kinase–knockout mice mitigates podocyte injury
Tian X, Inoue K, Zhang Y, Wang Y, Sperati CJ, Pedigo CE, Zhao T, Yan M, Groener M, Moledina DG, Ebenezer K, Li W, Zhang Z, Liebermann D, Greene L, Greer P, Parikh CR, Ishibe S. Inhibiting calpain 1 and 2 in cyclin G associated kinase–knockout mice mitigates podocyte injury. JCI Insight 2020, 5: e142740. PMID: 33208557, PMCID: PMC7710277, DOI: 10.1172/jci.insight.142740.Peer-Reviewed Original ResearchConceptsCalpain-1Chronic kidney diseaseDegree of proteinuriaCalpain inhibitor IIIGlomeruli of patientsProgressive proteinuriaCalpain protease activityGlobal glomerulosclerosisGlomerular injuryKidney functionKidney diseaseKidney failureCalcium dysregulationPodocyte injuryPodocyte-specific deletionPodocyte damageG associated kinaseProtective roleCalpain activationProteinuriaGlomerulosclerosisMiceReduced expressionStriking increaseInjuryProtective Role of Tangshen Formula on the Progression of Renal Damage in db/db Mice by TRPC6/Talin1 Pathway in Podocytes
Wang Q, Tian X, Zhou W, Wang Y, Zhao H, Li J, Zhou X, Zhang H, Zhao T, Li P. Protective Role of Tangshen Formula on the Progression of Renal Damage in db/db Mice by TRPC6/Talin1 Pathway in Podocytes. Journal Of Diabetes Research 2020, 2020: 3634974. PMID: 33015191, PMCID: PMC7519445, DOI: 10.1155/2020/3634974.Peer-Reviewed Original ResearchMeSH KeywordsActinsAnimalsCell AdhesionCell MovementCell SurvivalCytoskeletonDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2Disease ProgressionDrugs, Chinese HerbalHumansKidney DiseasesKidney GlomerulusMaleMedicine, Chinese TraditionalMiceMice, Inbred C57BLPodocytesProteinuriaTalinTRPC6 Cation ChannelWound HealingConceptsDiabetic kidney diseasePrimary mouse podocytesTangshen FormulaTransient receptor potential canonical channel 6Renal functionKidney diseaseTSF treatmentMouse podocytesType 2 diabetic kidney diseaseProtective roleDb/db miceAdvanced glycation end productsTRPC6-dependent CaProteinuric kidney diseaseActivated T cells 2Chinese medicine formulaGlycation end productsExpression of Talin1T cells 2Foot process effacementLoss of talin1Renal damageDb micePodocyte numberMurine modelIdiopathic Membranous Nephropathy: Glomerular Pathological Pattern Caused by Extrarenal Immunity Activity
Liu W, Gao C, Liu Z, Dai H, Feng Z, Dong Z, Zheng Y, Gao Y, Tian X, Liu B. Idiopathic Membranous Nephropathy: Glomerular Pathological Pattern Caused by Extrarenal Immunity Activity. Frontiers In Immunology 2020, 11: 1846. PMID: 33042109, PMCID: PMC7524879, DOI: 10.3389/fimmu.2020.01846.BooksConceptsIdiopathic membranous nephropathyGlomerular lesionsThrombospondin type-1 domain-containing 7APathological patternsImmune complex depositionDevelopment of proteinuriaM-type receptorNeural epidermal growthSecretory phospholipase A2Glomerular basement membraneIgG4 predominanceProteinuria remissionCirculating AntibodiesClinical featuresGlomerular damageMembranous nephropathySpontaneous remissionAutoimmune responseComplex depositionExtrarenal tissuesImmune activityAutoimmunity initiationClinical practicePathogenesis modelTHSD7A antigenEstablishment of a novel nomogram for the clinically diagnostic prediction of minimal change disease, −a common cause of nephrotic syndrome
Yan G, Liu G, Tian X, Tian L, Wang H, Ren P, Ma X, Fu R, Chen Z. Establishment of a novel nomogram for the clinically diagnostic prediction of minimal change disease, −a common cause of nephrotic syndrome. BMC Nephrology 2020, 21: 396. PMID: 32928127, PMCID: PMC7490860, DOI: 10.1186/s12882-020-02058-3.Peer-Reviewed Original ResearchMeSH KeywordsAdultArea Under CurveBlood PressureComplement C1qComplement C3Complement C4DiastoleFemaleGlomerular Filtration RateHemoglobinsHumansImmunoglobulin EImmunoglobulin GImmunoglobulin MMaleMiddle AgedNephrosis, LipoidNephrotic SyndromeNomogramsRegression AnalysisReproducibility of ResultsSensitivity and SpecificityYoung AdultConceptsDiastolic blood pressurePrimary glomerular diseaseNephrotic syndromeAdult patientsRenal biopsyChange diseaseGlomerular diseaseBackgroundMinimal change diseaseMinimal change diseaseLASSO regression analysisRenal biopsy procedureNon-MCD groupLogistic regression modelsDiagnostic prediction modelNovel nomogramPatient demographicsBlood pressureSerum levelsOverall incidenceClinical manifestationsMCD patientsMCD diagnosisCommon causeInvasive proceduresMethodA totalRole of Transient Receptor Potential Canonical Channel 6 (TRPC6) in Diabetic Kidney Disease by Regulating Podocyte Actin Cytoskeleton Rearrangement
Wang Q, Tian X, Wang Y, Wang Y, Li J, Zhao T, Li P. Role of Transient Receptor Potential Canonical Channel 6 (TRPC6) in Diabetic Kidney Disease by Regulating Podocyte Actin Cytoskeleton Rearrangement. Journal Of Diabetes Research 2020, 2020: 6897390. PMID: 31998809, PMCID: PMC6964719, DOI: 10.1155/2020/6897390.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsDiabetic kidney diseaseTransient receptor potential canonical channel 6Proteinuric kidney diseaseKidney diseaseMechanisms of DKDMultiple pathogenic factorsActin cytoskeleton rearrangementNew therapeutic targetsCytoskeleton rearrangementDKD patientsChannel 6Glomerular injuryPodocyte injuryPathogenic factorsTherapeutic targetDiseaseInjuryPodocytesCritical rolePatientsProgression
2019
Podocyte histone deacetylase activity regulates murine and human glomerular diseases
Inoue K, Gan G, Ciarleglio M, Zhang Y, Tian X, Pedigo CE, Cavanaugh C, Tate J, Wang Y, Cross E, Groener M, Chai N, Wang Z, Justice A, Zhang Z, Parikh CR, Wilson FP, Ishibe S. Podocyte histone deacetylase activity regulates murine and human glomerular diseases. Journal Of Clinical Investigation 2019, 129: 1295-1313. PMID: 30776024, PMCID: PMC6391095, DOI: 10.1172/jci124030.Peer-Reviewed Original ResearchConceptsEarly growth response 1Histone deacetylase 1Proteinuric patientsKidney diseaseHDAC2 activityValproic acidVeterans Aging Cohort StudyEnd-stage kidney diseaseDegree of proteinuriaGlomerular filtration rateAging Cohort StudyInhibition of HDAC1Proteinuric kidney diseaseHuman glomerular diseasesGlomerular disease modelsConnectivity Map databaseCohort studyFiltration rateGlomerular diseaseHistone deacetylase activityProteinuric kidneysHDAC inhibitorsProteinuriaMRNA expressionGenetic ablation
2016
Kidney Tubular Ablation of Ocrl/Inpp5b Phenocopies Lowe Syndrome Tubulopathy
Inoue K, Balkin DM, Liu L, Nandez R, Wu Y, Tian X, Wang T, Nussbaum R, De Camilli P, Ishibe S. Kidney Tubular Ablation of Ocrl/Inpp5b Phenocopies Lowe Syndrome Tubulopathy. Journal Of The American Society Of Nephrology 2016, 28: 1399-1407. PMID: 27895154, PMCID: PMC5407733, DOI: 10.1681/asn.2016080913.Peer-Reviewed Original ResearchConceptsEarly embryonic lethalityTransporter 5Dent's diseaseIndependent endocytosisEmbryonic lethalityRedundant functionsType 2 inositolHuman phenotypesProximal tubule endocytosisOculocerebrorenal syndromeGenetic ablationCellular levelGermline knockoutLowe syndromeEndocytosisMouse backgroundMice resultsMutationsInositolLow molecular weight proteinuriaINPP5BParalogsProximal tubule functionDramatic effectOCRLTargeting the podocyte cytoskeleton: from pathogenesis to therapy in proteinuric kidney disease
Tian X, Ishibe S. Targeting the podocyte cytoskeleton: from pathogenesis to therapy in proteinuric kidney disease. Nephrology Dialysis Transplantation 2016, 31: 1577-1583. PMID: 26968197, PMCID: PMC5039341, DOI: 10.1093/ndt/gfw021.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsProteinuric kidney diseaseKidney diseaseGlomerular filtration barrierChronic kidney diseaseLack of therapyFiltration barrierIntact glomerular filtration barrierMillions of patientsImportance of podocytesHuman nephrotic syndromeGlomerular injuryNephrotic syndromeTherapeutic implicationsTherapeutic targetPodocyte actin cytoskeletonDisease pathogenesisExciting new dataPathogenesisEpithelial cellsGenetic mutationsDiseasePodocyte cytoskeletonTherapyProgressionPodocytes
2014
Podocyte-associated talin1 is critical for glomerular filtration barrier maintenance
Tian X, Kim JJ, Monkley SM, Gotoh N, Nandez R, Soda K, Inoue K, Balkin DM, Hassan H, Son SH, Lee Y, Moeckel G, Calderwood DA, Holzman LB, Critchley DR, Zent R, Reiser J, Ishibe S. Podocyte-associated talin1 is critical for glomerular filtration barrier maintenance. Journal Of Clinical Investigation 2014, 124: 1098-1113. PMID: 24531545, PMCID: PMC3934159, DOI: 10.1172/jci69778.Peer-Reviewed Original ResearchConceptsNephrotic syndromeFoot process effacementLoss of talin1Glomerular filtration barrierGlomerular injuryMurine modelProcess effacementKidney's glomerular filtration barrierFiltration barrierGlomerular basement membraneSevere proteinuriaKidney failurePharmacologic inhibitionSyndromeBarrier maintenanceCalpain activityIntegrin activationEpithelial cellsPodocytesModest reductionΒ1 integrin activationBasement membranePathogenesisInjuryCytoskeletal protein talin1