2024
Understanding 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 cellsCase report: Genotype-phenotype characteristics of nine novel PKD1 mutations in eight Chinese patients with autosomal dominant polycystic kidney disease
Zhuang J, Aierken A, Yalikun D, Zhang J, Wang X, Ren Y, Tian X, Jiang H. Case report: Genotype-phenotype characteristics of nine novel PKD1 mutations in eight Chinese patients with autosomal dominant polycystic kidney disease. Frontiers In Medicine 2023, 10: 1268307. PMID: 37901409, PMCID: PMC10600478, DOI: 10.3389/fmed.2023.1268307.Peer-Reviewed Case Reports and Technical NotesAutosomal dominant polycystic kidney diseaseDominant polycystic kidney diseaseKidney diseasePolycystic kidney diseaseWhole-exome sequencingNovel mutation sitesDisease progressionNovel PKD1 mutationChronic kidney diseaseRapid disease progressionGene mutationsGenotype-phenotype characteristicsPeripheral blood DNAPersonalized therapeutic strategiesAge of onsetMilder disease phenotypeCommon genetic disorderAutosomal dominant inheritancePolycystic liverADPKD patientsChinese patientsClinical dataTherapeutic strategiesClinical phenotypeEarly onsetAdvances 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 studies
2022
New insights into the role of dipeptidyl peptidase 8 and dipeptidyl peptidase 9 and their inhibitors
Cui C, Tian X, Wei L, Wang Y, Wang K, Fu R. New insights into the role of dipeptidyl peptidase 8 and dipeptidyl peptidase 9 and their inhibitors. Frontiers In Pharmacology 2022, 13: 1002871. PMID: 36172198, PMCID: PMC9510841, DOI: 10.3389/fphar.2022.1002871.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsDipeptidyl peptidase 8Peptidase 8Dipeptidyl peptidase 9Serine proteolytic enzymesBiological processesNew potential targetsPhysiological functionsSpecific substratesCell behaviorNormal developmentEnergy metabolismEssential roleChronic kidney diseaseN-terminal dipeptidePenultimate positionPotential targetOrgan fibrosisPathological rolePathological processesNew insightsTreatment of tumorsProteolytic enzymesRecent research advancesKidney diseaseCell pyroptosis
2021
New Insights into the Immunity and Podocyte in Glomerular Health and Disease: From Pathogenesis to Therapy in Proteinuric Kidney Disease
Medina Rangel P, Priyadarshini A, Tian X. New Insights into the Immunity and Podocyte in Glomerular Health and Disease: From Pathogenesis to Therapy in Proteinuric Kidney Disease. Integrative Medicine In Nephrology And Andrology 2021, 8: 5. DOI: 10.4103/imna.imna_26_21.Peer-Reviewed Original ResearchProteinuric kidney diseaseKidney diseaseGlomerular injuryPodocyte injuryChronic kidney diseaseMillions of patientsAdaptive immune systemGlomerular filtration barrierImmune cellsImmune mechanismsTherapeutic implicationsTherapeutic targetGlomerular healthImmune systemInjuryComplement componentsDiseaseEpithelial cellsPodocytesFiltration barrierPresent reviewRecent findingsRecent studiesCellsPatientsCase Report: The Monogenic Familial Steroid-Resistant Nephrotic Syndrome Caused by a Novel Missense Mutation of NPHS2 Gene A593C in a Chinese Family
Bai L, Zhuang J, Zhang C, Lu C, Tian X, Jiang H. Case Report: The Monogenic Familial Steroid-Resistant Nephrotic Syndrome Caused by a Novel Missense Mutation of NPHS2 Gene A593C in a Chinese Family. Frontiers In Pediatrics 2021, 9: 692727. PMID: 34631609, PMCID: PMC8497038, DOI: 10.3389/fped.2021.692727.Peer-Reviewed Case Reports and Technical NotesSteroid-resistant nephrotic syndromeEnd-stage kidney diseaseFocal segmental glomerulosclerosisNephrotic syndromeHeterozygous asymptomatic carriersRenal pathological lesionsGene variantsTrio whole-exome sequencingPrediction of prognosisAutosomal recessive steroid-resistant nephrotic syndromeWhole-exome sequencingMissense mutationsRituximab treatmentProgressive proteinuriaGlomerular filtration barrierMale patientsCalcineurin inhibitorsKidney diseaseAsymptomatic carriersSegmental glomerulosclerosisHemodialysis treatmentTreatment strategiesFamilial steroid-resistant nephrotic syndromePathological lesionsConsanguineous Chinese family
2020
Inhibiting 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 modelRole 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 rolePatientsProgressionAlleviation by Mahuang Fuzi and Shenzhuo Decoction in High Glucose‐Induced Podocyte Injury by Inhibiting the Activation of Wnt/β‐Catenin Signaling Pathway, Resulting in Activation of Podocyte Autophagy
Dai H, Liu F, Qiu X, Liu W, Dong Z, Jia Y, Feng Z, Liu Z, Zhao Q, Gao Y, Zhang Z, Gao C, Sun S, Tian X, Liu B. Alleviation by Mahuang Fuzi and Shenzhuo Decoction in High Glucose‐Induced Podocyte Injury by Inhibiting the Activation of Wnt/β‐Catenin Signaling Pathway, Resulting in Activation of Podocyte Autophagy. Evidence-based Complementary And Alternative Medicine 2020, 2020: 7809427. PMID: 32963573, PMCID: PMC7486640, DOI: 10.1155/2020/7809427.Peer-Reviewed Original ResearchDiabetic kidney diseaseHigh glucose-induced podocytesMahuang-FuziPodocyte injuryExcessive activationProtein expressionTreatment of DKDHigh glucoseTraditional Chinese medicine compoundWnt/β-Catenin Signaling PathwayInjury-related proteinsChinese medicine compoundΒ-Catenin Signaling PathwayPathway-related proteinsHigh glucose stimulationInhibition of autophagyKidney diseaseVariety of diseasesPodocyte autophagyFuzi decoctionOrgan fibrosisMetabolic diseasesGolden ChamberInhibitor DKK1Western blotting
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
Targeting 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