Emma Ristori, PhD
Cards
About
Research
Publications
2024
Disruption 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
ALDH1A1 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 cellsAuthor 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. DOI: 10.1038/s44161-022-00092-y.Peer-Reviewed Original ResearchSyndecan-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 stimuliExpressionNew Insights Into Blood-Brain Barrier Maintenance: The Homeostatic Role of β-Amyloid Precursor Protein in Cerebral Vasculature
Ristori E, Donnini S, Ziche M. New Insights Into Blood-Brain Barrier Maintenance: The Homeostatic Role of β-Amyloid Precursor Protein in Cerebral Vasculature. Frontiers In Physiology 2020, 11: 1056. PMID: 32973564, PMCID: PMC7481479, DOI: 10.3389/fphys.2020.01056.Peer-Reviewed Original ResearchCerebral amyloid angiopathyΒ-amyloid precursor proteinBlood-brain barrierCentral nervous systemAlzheimer's diseaseBlood-brain barrier maintenanceΒ-amyloid accumulationPeripheral blood circulationPrecursor proteinEndothelial cell homeostasisCAA pathogenesisBBB dysfunctionBBB functionAmyloid angiopathyVascular dysfunctionAD onsetCerebrovascular homeostasisCerebral vasculatureVascular endotheliumPathological outcomesNervous systemHomeostatic roleBrain vasculatureNeurodegenerative disordersBarrier maintenanceCommon Protective Strategies in Neurodegenerative Disease: Focusing on Risk Factors to Target the Cellular Redox System
Hrelia P, Sita G, Ziche M, Ristori E, Marino A, Cordaro M, Molteni R, Spero V, Malaguti M, Morroni F, Hrelia S. Common Protective Strategies in Neurodegenerative Disease: Focusing on Risk Factors to Target the Cellular Redox System. Oxidative Medicine And Cellular Longevity 2020, 2020: 8363245. PMID: 32832006, PMCID: PMC7422410, DOI: 10.1155/2020/8363245.Peer-Reviewed Original ResearchConceptsNeurodegenerative diseasesRisk factorsCellular redox systemsRedox homeostasisMolecular mechanismsMultiple risk factorsPivotal risk factorComplex multifactorial natureDisease mechanismsVascular injuryChronic neurodegenerationPreventive strategiesCommon mechanismOxidative stressMultifactorial natureDiseaseProtective strategiesHuman brainRedox systemProgressionComplex networksMechanismHomeostasisEarly stagesInflammation