2023
Nonpodocyte Roles of APOL1 Variants: An Evolving Paradigm
Pell J, Nagata S, Menon M. Nonpodocyte Roles of APOL1 Variants: An Evolving Paradigm. Kidney360 2023, 4: e1325-e1331. PMID: 37461136, PMCID: PMC10550003, DOI: 10.34067/kid.0000000000000216.Peer-Reviewed Original ResearchConceptsApolipoprotein L1Progressive renal failureAPOL1 risk variantsImmune response genesParadigm of diseasesMechanisms of diseaseRenal failureKidney diseaseBody of evidenceImmune cellsClinical dataRecent African ancestryRisk genotypesAPOL1 variantsDiseaseEndothelial cellsPutative signaling pathwaysGenetic factorsSeminal dataPhenotype progressionCausal rolePodocytesRisk variantsSignaling pathwaysEvolving ParadigmHCK 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
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