Featured Publications
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
2016
Mitochondrial Redox Signaling and Tumor Progression
Chen Y, Zhang H, Zhou HJ, Ji W, Min W. Mitochondrial Redox Signaling and Tumor Progression. Cancers 2016, 8: 40. PMID: 27023612, PMCID: PMC4846849, DOI: 10.3390/cancers8040040.Peer-Reviewed Original ResearchMitochondrial redox proteinsExcessive ROSRedox proteinsCancer cellsMitochondrial redox signalingMitochondrial oxidative phosphorylationCellular ROS levelsStress signalingRedox regulationROS functionTumor progressionRedox signalingMitochondrial roleApoptotic signalingCancer cell proliferationRedox-sensitive pathwaysTranscriptional factorsReactive oxygen species generationTumor suppressorOxidative phosphorylationDNA mutationsOxygen species generationCancer progressionBasal ROSCancer invasion