Emma Ristori, PhD
Associate Research Scientist (Cardiovascular Medicine)Cards
About
Research
Publications
2025
Anti-Syndecan 2 Antibody Treatment Reduces Edema Formation and Inflammation of Murine Laser-Induced CNV.
Corti F, Locri F, Plastino F, Perrotta P, Zsebo K, Ristori E, Yin X, Song E, André H, Simons M. Anti-Syndecan 2 Antibody Treatment Reduces Edema Formation and Inflammation of Murine Laser-Induced CNV. Translational Vision Science & Technology 2025, 14: 10. PMID: 39792057, PMCID: PMC11730891, DOI: 10.1167/tvst.14.1.10.Peer-Reviewed Original ResearchConceptsAge-related macular degenerationLaser-induced choroidal neovascularizationAnti-VEGF therapyTransendothelial electrical resistanceVEGF-A activityChoroidal neovascularizationIntravitreal injectionRetinal lesionsLong-term anti-VEGF therapyMurine laser-induced choroidal neovascularizationNeovascular age-related macular degenerationWet age-related macular degenerationAlteration of visual acuityIntravitreal anti-VEGF therapySide effectsLocal intravitreal injectionReduced edema formationSuppression of edemaRelated side effectsPermeability in vitroEndothelial cell junctionsNeovascular AMDVisual acuityAssessed in vitroMacular degeneration
2024
Akt is a mediator of artery specification during zebrafish development
Zhou W, Ghersi J, Ristori E, Semanchik N, Prendergast A, Zhang R, Carneiro P, Baldissera G, Sessa W, Nicoli S. Akt is a mediator of artery specification during zebrafish development. Development 2024, 151: dev202727. PMID: 39101673, PMCID: PMC11441982, DOI: 10.1242/dev.202727.Peer-Reviewed Original ResearchArterial specificationEndothelial cellsVascular endothelial growth factor ADorsal aortaEndothelial growth factor ASingle-cell RNA sequencing analysisGrowth factor AArtery endothelial cellsEmbryonic cardiovascular systemConstitutively active Akt1Ligand-independent activationActivation of NotchArteriovenous malformationsCongenital malformationsRNA sequencing analysisVEGF-AProtein kinase BUpstream of NotchSequence analysisCardiovascular developmentSpecific expressionAkt kinaseActive Akt1Zebrafish developmentCardiovascular systemDisruption of mitochondrial unfolded protein response results in telomere shortening in mouse oocytes and somatic cells
Cozzolino M, Ergun Y, Ristori E, Garg A, Imamoglu G, Seli E. Disruption of mitochondrial unfolded protein response results in telomere shortening in mouse oocytes and somatic cells. Aging 2024, 16: 2047-2060. PMID: 38349865, PMCID: PMC10911389, DOI: 10.18632/aging.205543.Peer-Reviewed Original ResearchConceptsCaseinolytic peptidase PMitochondrial unfolded protein responseUnfolded protein responseTelomere integrityProtein responseGermline deletionSomatic cellsSomatic agingSomatic cell divisionDouble-stranded DNA breaksAged miceTelomere shorteningAssociated with cellular senescenceTelomeric regionsProtein homeostasisAccelerated follicular depletionChromosome stabilityCell divisionMtUPRDNA breaksTelomereAging phenotypesCellular senescenceFollicular depletionMouse oocytes
2022
Author Correction: Syndecan-2 selectively regulates VEGF-induced vascular permeability
Corti F, Ristori E, Rivera-Molina F, Toomre D, Zhang J, Mihailovic J, Zhuang Z, Simons M. Author Correction: Syndecan-2 selectively regulates VEGF-induced vascular permeability. Nature Cardiovascular Research 2022, 1: 592-592. PMID: 39195875, DOI: 10.1038/s44161-022-00092-y.Peer-Reviewed Original ResearchALDH1A1 overexpression in melanoma cells promotes tumor angiogenesis by activating the IL-8/Notch signaling cascade
Ciccone V, Terzuoli E, Ristori E, Filippelli A, Ziche M, Morbidelli L, Donnini S. ALDH1A1 overexpression in melanoma cells promotes tumor angiogenesis by activating the IL-8/Notch signaling cascade. International Journal Of Molecular Medicine 2022, 50: 99. PMID: 35656893, PMCID: PMC9186295, DOI: 10.3892/ijmm.2022.5155.Peer-Reviewed Original ResearchConceptsIL-8Endothelial cellsMelanoma cellsTumor cellsALDH1A1 expressionAngiogenic factorsAngiogenic featuresTumor microenvironmentCancer cellsPoor clinical outcomeHigher microvessel densityNumber of cancersPro-angiogenic phenotypeOverexpression of ALDH1A1ALDH1A1 overexpressionClinical outcomesCo-culture systemMicrovessel densityImmunodeficient miceNF-kBProangiogenic factorsMelanoma cancer cellsTumor angiogenesisMelanoma controlStromal cellsSyndecan-2 selectively regulates VEGF-induced vascular permeability
Corti F, Ristori E, Rivera-Molina F, Toomre D, Zhang J, Mihailovic J, Zhuang ZW, Simons M. Syndecan-2 selectively regulates VEGF-induced vascular permeability. Nature Cardiovascular Research 2022, 1: 518-528. PMID: 36212522, PMCID: PMC9544384, DOI: 10.1038/s44161-022-00064-2.Peer-Reviewed Original ResearchChapter 2 Antiangiogenic drugs: Chemosensitizers for combination cancer therapy
Donnini S, Filippelli A, Ciccone V, Spini A, Ristori E, Ziche M, Morbidelli L. Chapter 2 Antiangiogenic drugs: Chemosensitizers for combination cancer therapy. 2022, 29-66. DOI: 10.1016/b978-0-323-90190-1.00008-1.Peer-Reviewed Original ResearchImmune-competent T cellsAntiangiogenic drugsVascular normalizationT cellsTumor vasculatureTumor microenvironmentTumor areaImmune checkpoint inhibitorsAnticancer drugsCheckpoint inhibitorsImmune therapyAdvanced tumorsCombination therapyPromising chemosensitizerAntiangiogenic therapyTarget therapyTumor disseminationAnticancer chemoClinical developmentEffective deliverySolid tumorsTherapyTumor progressionTumor resistanceTumor angiogenesis
2021
PPIL4 is essential for brain angiogenesis and implicated in intracranial aneurysms in humans
Barak T, Ristori E, Ercan-Sencicek AG, Miyagishima DF, Nelson-Williams C, Dong W, Jin SC, Prendergast A, Armero W, Henegariu O, Erson-Omay EZ, Harmancı AS, Guy M, Gültekin B, Kilic D, Rai DK, Goc N, Aguilera SM, Gülez B, Altinok S, Ozcan K, Yarman Y, Coskun S, Sempou E, Deniz E, Hintzen J, Cox A, Fomchenko E, Jung SW, Ozturk AK, Louvi A, Bilgüvar K, Connolly ES, Khokha MK, Kahle KT, Yasuno K, Lifton RP, Mishra-Gorur K, Nicoli S, Günel M. PPIL4 is essential for brain angiogenesis and implicated in intracranial aneurysms in humans. Nature Medicine 2021, 27: 2165-2175. PMID: 34887573, PMCID: PMC8768030, DOI: 10.1038/s41591-021-01572-7.Peer-Reviewed Original ResearchConceptsGenome-wide association studiesPeptidyl-prolyl cis-transPathogenesis of IAContribution of variantsCommon genetic variantsVertebrate modelDeleterious mutationsWnt activatorAssociation studiesWhole-exome sequencingSignificant enrichmentGenetic variantsWntAngiogenesis regulatorsMutationsGene mutationsBrain angiogenesisIntracranial aneurysm ruptureJMJD6AngiogenesisCerebrovascular morphologyCerebrovascular integrityIntracerebral hemorrhageAneurysm ruptureVariantsMITOCHONDRIAL DYSFUNCTION CAUSED BY TARGETED DELETION OF CLPP Results IN TELOMERE SHORTENING IN OOCYTES AND SOMATIC CELLS
Cozzolino M, Imamoglu G, Ristori E, Seli E. MITOCHONDRIAL DYSFUNCTION CAUSED BY TARGETED DELETION OF CLPP Results IN TELOMERE SHORTENING IN OOCYTES AND SOMATIC CELLS. Fertility And Sterility 2021, 116: e411. DOI: 10.1016/j.fertnstert.2021.07.1101.Peer-Reviewed Original Research
2020
Amyloid-β Precursor Protein APP Down-Regulation Alters Actin Cytoskeleton-Interacting Proteins in Endothelial Cells
Ristori E, Cicaloni V, Salvini L, Tinti L, Tinti C, Simons M, Corti F, Donnini S, Ziche M. Amyloid-β Precursor Protein APP Down-Regulation Alters Actin Cytoskeleton-Interacting Proteins in Endothelial Cells. Cells 2020, 9: 2506. PMID: 33228083, PMCID: PMC7699411, DOI: 10.3390/cells9112506.Peer-Reviewed Original ResearchConceptsAmyloid-β precursor proteinCerebral amyloid angiopathyUbiquitous membrane proteinsFocal adhesion stabilityEndothelial cellsMajor cellular targetInteracting proteinActin cytoskeletonProteomic approachMembrane proteinsAlzheimer's diseaseMolecular mechanismsCellular responsesCellular targetsPhysiological roleRole of APPEndothelial cell proliferationPrecursor proteinCell proliferationNormal endothelial functionProteinNeuronal tissueGrowth factorExogenous stimuliExpression
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