2023
HCK induces macrophage activation to promote renal inflammation and fibrosis via suppression of autophagy
Chen M, Menon M, Wang W, Fu J, Yi Z, Sun Z, Liu J, Li Z, Mou L, Banu K, Lee S, Dai Y, Anandakrishnan N, Azeloglu E, Lee K, Zhang W, Das B, He J, Wei C. HCK induces macrophage activation to promote renal inflammation and fibrosis via suppression of autophagy. Nature Communications 2023, 14: 4297. PMID: 37463911, PMCID: PMC10354075, DOI: 10.1038/s41467-023-40086-3.Peer-Reviewed Original ResearchConceptsChronic kidney diseasePro-inflammatory polarizationBone marrow-derived macrophagesRenal inflammationKidney fibrosisMacrophage activationHematopoietic cell kinaseMacrophage pro-inflammatory activityProgressive chronic kidney diseaseIschemia-reperfusion injury modelUnilateral ureteral obstruction kidneysChronic allograft injuryReperfusion injury modelPro-inflammatory activityPro-inflammatory macrophagesHck inhibitorsMarrow-derived macrophagesSuppression of autophagyAllograft injuryUUO miceRenal fibrosisKidney diseaseDiseased kidneysMacrophage numbersInjury model
2020
Genome-wide non-HLA donor-recipient genetic differences influence renal allograft survival via early allograft fibrosis
Zhang Z, Menon MC, Zhang W, Stahl E, Loza BL, Rosales IA, Yi Z, Banu K, Garzon F, Sun Z, Wei C, Huang W, Lin Q, Israni A, Keating BJ, Colvin RB, Hao K, Murphy B. Genome-wide non-HLA donor-recipient genetic differences influence renal allograft survival via early allograft fibrosis. Kidney International 2020, 98: 758-768. PMID: 32454123, PMCID: PMC7483801, DOI: 10.1016/j.kint.2020.04.039.Peer-Reviewed Original ResearchConceptsAllograft survivalIntimal fibrosisDeath-censored allograft survivalLong-term allograft failureAcute rejection episodesDonor-recipient differencesRenal allograft survivalHuman leukocyte antigen (HLA) lociNon-HLA SNPsLong-term survivalAllograft failureHLA mismatchesKidney recipientsRejection episodesSubclinical rejectionAllograft fibrosisMultivariable analysisHistologic damageR differencesOrgan SharingCox modelFibrosisHLA regionSurvivalGenome-wide single-nucleotide polymorphism array data
2019
Multiparametric magnetic resonance imaging shows promising results to assess renal transplant dysfunction with fibrosis
Bane O, Hectors S, Gordic S, Kennedy P, Wagner M, Weiss A, Khaim R, Yi Z, Zhang W, Delaney V, Salem F, He C, Menon MC, Lewis S, Taouli B. Multiparametric magnetic resonance imaging shows promising results to assess renal transplant dysfunction with fibrosis. Kidney International 2019, 97: 414-420. PMID: 31874802, PMCID: PMC6983343, DOI: 10.1016/j.kint.2019.09.030.Peer-Reviewed Original ResearchConceptsCortical apparent diffusion coefficientApparent diffusion coefficientChronic dysfunctionMedullary apparent diffusion coefficientsProspective single-center studyFractional anisotropyMultiparametric magnetic resonance imagingRenal allograft histologyRenal transplant dysfunctionTubular atrophy scoreRenal allograft dysfunctionRenal transplant patientsSingle-center studyMagnetic resonance imaging protocolIntravoxel incoherent motion diffusion-weighted imagingNon-invasive assessmentTest-retest repeatabilityMagnetic resonance imagingDiffusion-weighted imagingBlood oxygen levelDiffusion tensor imagingInter-observer reproducibilityAllograft dysfunctionAllograft histologyEGFR decline
2016
Biopsy transcriptome expression profiling to identify kidney transplants at risk of chronic injury: a multicentre, prospective study
O'Connell PJ, Zhang W, Menon MC, Yi Z, Schröppel B, Gallon L, Luan Y, Rosales IA, Ge Y, Losic B, Xi C, Woytovich C, Keung KL, Wei C, Greene I, Overbey J, Bagiella E, Najafian N, Samaniego M, Djamali A, Alexander SI, Nankivell BJ, Chapman JR, Smith RN, Colvin R, Murphy B. Biopsy transcriptome expression profiling to identify kidney transplants at risk of chronic injury: a multicentre, prospective study. The Lancet 2016, 388: 983-993. PMID: 27452608, PMCID: PMC5014570, DOI: 10.1016/s0140-6736(16)30826-1.Peer-Reviewed Original ResearchConceptsChronic allograft damage indexAllograft lossKidney transplantPathological variablesChronic injuryEarly allograft lossKidney transplant recipientsRenal allograft recipientsFunction 3 monthsBaseline clinical variablesDevelopment of fibrosisAllograft recipientsNormal allograftsRenal allograftsTransplant recipientsAllograft fibrosisMulticentre studyProgressive injuryProspective studyClinical variablesIndependent cohortLower riskFibrosisPredictive valueTransplant
2014
Intronic locus determines SHROOM3 expression and potentiates renal allograft fibrosis
Menon MC, Chuang PY, Li Z, Wei C, Zhang W, Luan Y, Yi Z, Xiong H, Woytovich C, Greene I, Overbey J, Rosales I, Bagiella E, Chen R, Ma M, Li L, Ding W, Djamali A, Saminego M, O’Connell P, Gallon L, Colvin R, Schroppel B, He JC, Murphy B. Intronic locus determines SHROOM3 expression and potentiates renal allograft fibrosis. Journal Of Clinical Investigation 2014, 125: 208-221. PMID: 25437874, PMCID: PMC4382250, DOI: 10.1172/jci76902.Peer-Reviewed Original ResearchMeSH KeywordsAllograftsAnimalsBeta CateninDisease SusceptibilityEnhancer Elements, GeneticFibrosisGene ExpressionGenetic Association StudiesGenetic LociHEK293 CellsHumansIntronsKidneyKidney DiseasesKidney TransplantationMaleMiceMicrofilament ProteinsPolymorphism, Single NucleotideQuantitative Trait LociRiskSmad3 ProteinTranscription Factor 7-Like 2 ProteinTranscriptional ActivationTransforming Growth Factor beta1ConceptsChronic allograft nephropathyChronic kidney diseaseAllograft fibrosisTGF-β1Development of CANRisk allelesKidney transplant recipientsRenal allograft recipientsGlomerular filtration rateRenal allograft fibrosisTGF-β1 administrationUnilateral ureteric obstructionRenal tubular cellsTranscription factor 7Canonical TGF-β1Cell-specific knockdownAllograft injuryAllograft nephropathyAllograft recipientsTransplant recipientsProspective cohortRenal functionInterstitial fibrosisUreteric obstructionKidney disease