2016
PI3 kinase inhibition improves vascular malformations in mouse models of hereditary haemorrhagic telangiectasia
Ola R, Dubrac A, Han J, Zhang F, Fang JS, Larrivée B, Lee M, Urarte AA, Kraehling JR, Genet G, Hirschi KK, Sessa WC, Canals FV, Graupera M, Yan M, Young LH, Oh PS, Eichmann A. PI3 kinase inhibition improves vascular malformations in mouse models of hereditary haemorrhagic telangiectasia. Nature Communications 2016, 7: 13650. PMID: 27897192, PMCID: PMC5141347, DOI: 10.1038/ncomms13650.Peer-Reviewed Original ResearchMeSH KeywordsActivin Receptors, Type IActivin Receptors, Type IIAnimalsBone Morphogenetic ProteinsDisease Models, AnimalGene DeletionHuman Umbilical Vein Endothelial CellsHumansMiceModels, BiologicalNeovascularization, PathologicPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProtein Kinase InhibitorsRetinaSignal TransductionTelangiectasia, Hereditary HemorrhagicVascular Endothelial Growth Factor Receptor-2Vascular MalformationsConceptsHereditary haemorrhagic telangiectasia type 2Activin receptor-like kinase 1Arteriovenous malformationsAVM formationAlk1 deletionPharmacological PI3K inhibitionExcessive angiogenesisSerine-threonine kinase receptorsBone morphogenetic protein 9PI3K pathway activationHereditary haemorrhagic telangiectasiaPI3-kinase inhibitionReceptor-like kinase 1PI3K/AktPI3K inhibitionVascular lesionsVascular malformationsGastrointestinal tractMouse modelProtein 9Type 2Kinase 1Retinal vesselsGenetic deletionALK1 gene
2015
AMPK is critical for mitochondrial function during reperfusion after myocardial ischemia
Zaha VG, Qi D, Su KN, Palmeri M, Lee HY, Hu X, Wu X, Shulman GI, Rabinovitch PS, Russell RR, Young LH. AMPK is critical for mitochondrial function during reperfusion after myocardial ischemia. Journal Of Molecular And Cellular Cardiology 2015, 91: 104-113. PMID: 26746142, PMCID: PMC4839186, DOI: 10.1016/j.yjmcc.2015.12.032.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisCatalaseGene Expression RegulationHydrogen PeroxideMAP Kinase Kinase 4MiceMice, Inbred C57BLMice, TransgenicMitochondria, HeartMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreMyocardial InfarctionMyocardial ReperfusionMyocardiumNecrosisProtein Kinase InhibitorsSignal TransductionTransgenesConceptsWild typeProtein kinase kinase 4Mitochondrial functionMitochondrial catalaseKinase-dead AMPKMitochondrial reactive oxygen productionStress-responsive kinaseMPTP openingC-Jun terminal kinaseInhibition of JNKPermeability transition pore openingMitochondrial permeability transition pore openingTransition pore openingAMPK inactivationResponsive kinaseTerminal kinaseCellular metabolismJNK activationMitochondrial integrityReactive oxygen productionTransgenic expressionCell survivalAMPKKinase 4Kinase