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 diseaseLoss 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
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