2024
Editorial: 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 Letters
2023
Advances 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 StatementsMeSH KeywordsDiabetes MellitusDiabetic NephropathiesFibrosisHumansInflammationKidney Failure, ChronicMineralocorticoid Receptor AntagonistsConceptsDiabetic 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
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 increaseInjuryRole 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 StatementsMeSH KeywordsActin CytoskeletonAnimalsDiabetic NephropathiesHumansKidney GlomerulusPodocytesTRPC6 Cation ChannelConceptsDiabetic 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