2022
Mitochondrial dysfunction induces ALK5-SMAD2-mediated hypovascularization and arteriovenous malformations in mouse retinas
Zhang H, Li B, Huang Q, López-Giráldez F, Tanaka Y, Lin Q, Mehta S, Wang G, Graham M, Liu X, Park I, Eichmann A, Min W, Zhou J. Mitochondrial dysfunction induces ALK5-SMAD2-mediated hypovascularization and arteriovenous malformations in mouse retinas. Nature Communications 2022, 13: 7637. PMID: 36496409, PMCID: PMC9741628, DOI: 10.1038/s41467-022-35262-w.Peer-Reviewed Original ResearchConceptsMitochondrial dysfunctionThioredoxin 2Single-cell RNA-seq analysisRNA-seq analysisMutant miceNuclear genesMitochondrial proteinsMitochondrial localizationHuman retinal diseasesTranscriptional factorsGene expressionMutant retinasMitochondrial activityExtracellular matrixNovel mechanismVascular maturationArteriovenous malformationsGenetic deficiencyVessel growthSmad2Mouse retinaVascular malformationsMechanistic studiesBasement membraneRetinal vascular malformations
2007
Biomechanical Gene Activation During Cardiovascular Development
Jones E, Le Noble F, Yuan L, Eichmann A. Biomechanical Gene Activation During Cardiovascular Development. The FASEB Journal 2007, 21: a201-a201. DOI: 10.1096/fasebj.21.5.a201-a.Peer-Reviewed Original ResearchCardiovascular developmentPhysical forcesGene activationEmbryonic developmentVenous differentiationBiochemical signalingMechanical cuesGene expressionEmbryo growthEphB4 receptorVascular formationNeuropilin-2Mechanical forcesNeuropilin-1Blood fluid dynamicsExternal stimuliGenesCardiovascular systemSignalingEmbryosEphrinB2DifferentiationRegulationDynamic interactionExpression