2020
Inhibition 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
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