2014
Chemokine receptor Cxcr4 contributes to kidney fibrosis via multiple effectors
Yuan A, Lee Y, Choi U, Moeckel G, Karihaloo A. Chemokine receptor Cxcr4 contributes to kidney fibrosis via multiple effectors. American Journal Of Physiology. Renal Physiology 2014, 308: f459-f472. PMID: 25537742, PMCID: PMC4346747, DOI: 10.1152/ajprenal.00146.2014.Peer-Reviewed Original ResearchConceptsUnilateral ureteral obstructionCXCR4 expressionKidney fibrosisChemokine receptorsFibrotic responseSmooth muscle actin levelsG protein-coupled chemokine receptorsGrowth factorChronic kidney inflammationProgressive tissue injuryChronic kidney diseaseHigh CXCR4 expressionTGF-β1 levelsEffector cell typesProgression of fibrosisScarring/fibrosisFinal common pathwayPlatelet-derived growth factorRenal injuryKidney inflammationObstructed kidneysBone morphogenetic protein-7Renal fibrosisUreteral obstructionKidney disease
2013
Macrophage-specific deletion of transforming growth factor-β1 does not prevent renal fibrosis after severe ischemia-reperfusion or obstructive injury
Huen SC, Moeckel GW, Cantley LG. Macrophage-specific deletion of transforming growth factor-β1 does not prevent renal fibrosis after severe ischemia-reperfusion or obstructive injury. American Journal Of Physiology. Renal Physiology 2013, 305: f477-f484. PMID: 23761668, PMCID: PMC3891258, DOI: 10.1152/ajprenal.00624.2012.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsFibrosisImmunoblottingKidneyKidney DiseasesMacrophagesMaleMiceReperfusion InjurySignal TransductionTransforming Growth Factor beta1ConceptsGrowth factor-β1Kidney injuryKidney diseaseRenal fibrosisTGF-β1Factor-β1Renal ischemia-reperfusion injuryChronic kidney diseaseIschemia-reperfusion injuryProgressive renal fibrosisMacrophage-specific deletionInnate immune responseMyeloid lineage cellsPersistence of macrophagesLater time pointsTubulointerstitial fibrosisFibrosis markersInterstitial fibrosisMacrophage infiltrationEffective therapyInjury modelObstructive injuryImmune responseTissue scarringFibrosis