2021
Podocyte Glucocorticoid Receptors Are Essential for Glomerular Endothelial Cell Homeostasis in Diabetes Mellitus
Srivastava SP, Zhou H, Setia O, Dardik A, Fernandez‐Hernando C, Goodwin J. Podocyte Glucocorticoid Receptors Are Essential for Glomerular Endothelial Cell Homeostasis in Diabetes Mellitus. Journal Of The American Heart Association 2021, 10: e019437. PMID: 34308664, PMCID: PMC8475689, DOI: 10.1161/jaha.120.019437.Peer-Reviewed Original ResearchConceptsDiabetic nephropathySegmental fibrosisFatty acid metabolismDiabetes mellitusEndothelial cellsPrimary podocytesReceptor knockout micePathogenesis of proteinuriaAdministration of streptozotocinProfibrotic gene expressionAcid metabolismGlomerular endothelial cellsSmooth muscle actinEndothelial cell homeostasisCarnitine palmitoyltransferase 1AFatty acid oxidationBackground ProteinuriaWorsened fibrosisClinical characteristicsFibrotic featuresGlomerular fibrosisGlomerular homeostasisPatient managementControl littermatesSevere diseaseInteractions among Long Non-Coding RNAs and microRNAs Influence Disease Phenotype in Diabetes and Diabetic Kidney Disease
Srivastava SP, Goodwin JE, Tripathi P, Kanasaki K, Koya D. Interactions among Long Non-Coding RNAs and microRNAs Influence Disease Phenotype in Diabetes and Diabetic Kidney Disease. International Journal Of Molecular Sciences 2021, 22: 6027. PMID: 34199672, PMCID: PMC8199750, DOI: 10.3390/ijms22116027.Peer-Reviewed Original ResearchMeSH KeywordsDiabetes MellitusDiabetic NephropathiesGene Expression RegulationHumansKidneyMicroRNAsPhenotypeRNA, Long NoncodingConceptsDiabetic kidney diseaseKidney diseaseLarge-scale RNA sequencingGenome-wide profiling dataLong non-coding RNAsNon-coding RNAsDisease phenotypeTherapeutic targetNoncoding RNAsRNA sequencingPathogenesis of diabetesPotential therapeutic targetCrosstalk mechanismsRegulatory microRNAsCrosstalk interactionsLncRNAsMechanism of actionProfiling dataMicroRNAsAberrant expressionDiverse targetsDisease processDiabetesRNADiseaseLoss of endothelial glucocorticoid receptor accelerates diabetic nephropathy
Srivastava SP, Zhou H, Setia O, Liu B, Kanasaki K, Koya D, Dardik A, Fernandez-Hernando C, Goodwin J. Loss of endothelial glucocorticoid receptor accelerates diabetic nephropathy. Nature Communications 2021, 12: 2368. PMID: 33888696, PMCID: PMC8062600, DOI: 10.1038/s41467-021-22617-y.Peer-Reviewed Original ResearchMeSH KeywordsAdrenalectomyAnimalsDiabetes Mellitus, ExperimentalDiabetic NephropathiesEndothelial CellsEndotheliumEpithelial-Mesenchymal TransitionFatty AcidsFibrosisGlucocorticoidsHumansHypercholesterolemiaInterleukin-6Kidney TubulesMaleMiceMice, Knockout, ApoEOxidation-ReductionReceptors, GlucocorticoidStreptozocinWnt Signaling PathwayConceptsEndothelial glucocorticoid receptorGlucocorticoid receptorEndothelial cell homeostasisDiabetic miceRenal fibrosisEndothelial cellsMesenchymal transitionSevere renal fibrosisTubular epithelial cellsCell homeostasisFatty acid oxidationDiabetic controlDiabetic nephropathyAntifibrotic moleculesIL-6Kidney fibrosisMesenchymal activationRegulation of diseaseOrgan fibrosisAberrant cytokineFibrogenic phenotypeFibrosisMiceEpithelial cellsDefective regulation
2020
Metabolic reprogramming by N‐acetyl‐seryl‐aspartyl‐lysyl‐proline protects against diabetic kidney disease
Srivastava SP, Goodwin JE, Kanasaki K, Koya D. Metabolic reprogramming by N‐acetyl‐seryl‐aspartyl‐lysyl‐proline protects against diabetic kidney disease. British Journal Of Pharmacology 2020, 177: 3691-3711. PMID: 32352559, PMCID: PMC7393199, DOI: 10.1111/bph.15087.Peer-Reviewed Original ResearchConceptsACE inhibitorsDiabetic kidneyKidney fibrosisEffects of ACEIsEnd-stage renal diseaseDiabetic CD-1 miceKidney cell metabolismAbnormal glucose metabolismDiabetic kidney diseaseFirst-line drugsCD-1 miceMesenchymal transformationFatty acid oxidationMitochondrial fatty acid oxidationAntifibrotic mediatorsFatty acid metabolismDiabetic patientsRenal diseaseAntifibrotic mechanismsSevere fibrosisACE inhibitionKidney diseaseAntifibrotic actionReceptor antagonistC57BL6 miceInhibition of Angiotensin-Converting Enzyme Ameliorates Renal Fibrosis by Mitigating DPP-4 Level and Restoring Antifibrotic MicroRNAs
Srivastava SP, Goodwin JE, Kanasaki K, Koya D. Inhibition of Angiotensin-Converting Enzyme Ameliorates Renal Fibrosis by Mitigating DPP-4 Level and Restoring Antifibrotic MicroRNAs. Genes 2020, 11: 211. PMID: 32085655, PMCID: PMC7074526, DOI: 10.3390/genes11020211.Peer-Reviewed Original ResearchMeSH KeywordsAngiotensin Receptor AntagonistsAngiotensin-Converting Enzyme InhibitorsAnimalsCell LineDiabetes Mellitus, ExperimentalDiabetic NephropathiesDipeptidyl Peptidase 4Disease Models, AnimalDrug SynergismGene Expression RegulationHumansMiceMicroRNAsOligopeptidesSignal TransductionTransforming Growth Factor betaConceptsAngiotensin II receptor blockersRenal fibrosisDPP-4End-stage renal diseaseSubstrates of ACEDiabetic kidney diseaseEffect of ACEIII receptor blockersDPP-4 levelsTGFβ signalingAngiotensin converting enzymeChronic nephropathyReceptor blockersRenal diseaseKidney diseaseACEIEnzyme inhibitorsConventional drugsDownregulated expressionEndothelial cellsFibrosisInhibitory effectDrug 1MiR-29AcSDKP
2018
SIRT3 deficiency leads to induction of abnormal glycolysis in diabetic kidney with fibrosis
Srivastava SP, Li J, Kitada M, Fujita H, Yamada Y, Goodwin JE, Kanasaki K, Koya D. SIRT3 deficiency leads to induction of abnormal glycolysis in diabetic kidney with fibrosis. Cell Death & Disease 2018, 9: 997. PMID: 30250024, PMCID: PMC6155322, DOI: 10.1038/s41419-018-1057-0.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCarnitine O-PalmitoyltransferaseCell LineDiabetes Mellitus, ExperimentalDiabetic NephropathiesFibrosisGene Knockdown TechniquesGlucoseGlycolysisHumansHypoxia-Inducible Factor 1, alpha SubunitKidneyMiceMice, Inbred C57BLPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPyruvate KinaseSirtuin 3StreptozocinTransfectionTransforming Growth Factor beta2ConceptsDiabetic kidneyAbnormal glycolysisAberrant glycolysisSIRT3 suppressionMouse modelProgressive diabetic kidney diseaseDiabetic kidney diseaseDiabetic mouse modelAberrant glucose metabolismSIRT3 protein levelsSIRT3 siRNADiabetic miceKidney diseaseKidney fibrosisSystemic administrationFibrogenic pathwaysSIRT3 deficiencyGlucose metabolismTherapeutic targetFibrosisSIRT3 levelsHIF1α accumulationFibrogenic phenotypeKidneyGrowth factor