2021
Loss 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 regulationEndothelial SIRT3 regulates myofibroblast metabolic shifts in diabetic kidneys
Srivastava SP, Li J, Takagaki Y, Kitada M, Goodwin JE, Kanasaki K, Koya D. Endothelial SIRT3 regulates myofibroblast metabolic shifts in diabetic kidneys. IScience 2021, 24: 102390. PMID: 33981977, PMCID: PMC8086030, DOI: 10.1016/j.isci.2021.102390.Peer-Reviewed Original ResearchDiabetic kidney fibrosisDiabetic kidneyEndothelial cellsKidney fibrosisDefective metabolismRenal tubular epithelial cellsTubular epithelial cellsKidney functionDiabetic miceFibrogenic pathwaysFibrogenic processDisease processLoss of functionMesenchymal transitionKidneyMouse strainsEpithelial cellsGain of functionSIRT3Metabolic reprogrammingMesenchymal transformationFibrosisSIRT3 geneMetabolismCells
2020
Cancer Biology and Prevention in Diabetes
Srivastava SP, Goodwin JE. Cancer Biology and Prevention in Diabetes. Cells 2020, 9: 1380. PMID: 32498358, PMCID: PMC7349292, DOI: 10.3390/cells9061380.Peer-Reviewed Original ResearchConceptsDPP-4 inhibitorsMesenchymal transitionType II diabetes mellitusCancer biologySite-specific cancersDevelopment of hyperglycemiaAnti-diabetic therapyRisk of cancerDipeptidyl peptidase-4New therapeutic approachesPossible mechanistic linkMolecular pathological mechanismsDiabetes mellitusSGLT2 inhibitorsChronic inflammationCancer-causing mechanismsDiabetic conditionsTumor cell extravasationAntidiabetic drugsTherapeutic approachesEpidemiological dataPeptidase-4DiabetesPathological mechanismsGlucocorticoid receptor
2019
microRNA Crosstalk Influences Epithelial-to-Mesenchymal, Endothelial-to-Mesenchymal, and Macrophage-to-Mesenchymal Transitions in the Kidney
Srivastava SP, Hedayat A, Kanasaki K, Goodwin JE. microRNA Crosstalk Influences Epithelial-to-Mesenchymal, Endothelial-to-Mesenchymal, and Macrophage-to-Mesenchymal Transitions in the Kidney. Frontiers In Pharmacology 2019, 10: 904. PMID: 31474862, PMCID: PMC6707424, DOI: 10.3389/fphar.2019.00904.Peer-Reviewed Original ResearchMesenchymal transitionExcess extracellular matrixDiverse biological processesGrowth factor β receptorNon-coding nucleotidesMiR-29Fibrotic disease statesRole of microRNAsEndothelial cell homeostasisEpithelial cellsMicroRNA biosynthesisMesenchymal programGrowth factor βAberrant regulationEndothelial cellsCrosstalk mechanismsCell homeostasisBiological processesM2 phenotype macrophagesDipeptidyl peptidase-4Extracellular matrixBone marrow-derived monocytesIntegrin β1Novel therapeutic targetMesenchymal activation