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
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 ruptureVariants
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 stimuliExpressionCommon 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