2021
Interactions 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 processDiabetesRNADisease
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 miceCancer 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 ResearchMeSH KeywordsDiabetes MellitusEpithelial-Mesenchymal TransitionHumansHypoglycemic AgentsNeoplasmsPrevalenceReceptors, GlucocorticoidConceptsDPP-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