Search results for "Cellular senescence"

showing 10 items of 109 documents

Coffee silverskin extract protects against accelerated aging caused by oxidative agents

2016

Nowadays, coffee beans are almost exclusively used for the preparation of the beverage. The sustainability of coffee production can be achieved introducing new applications for the valorization of coffee by-products. Coffee silverskin is the by-product generated during roasting, and because of its powerful antioxidant capacity, coffee silverskin aqueous extract (CSE) may be used for other applications, such as antiaging cosmetics and dermaceutics. This study aims to contribute to the coffee sector’s sustainability through the application of CSE to preserve skin health. Preclinical data regarding the antiaging properties of CSE employing human keratinocytes and Caenorhabditis elegans are col…

0301 basic medicineAgingAntioxidantmedicine.medical_treatmentdermaceuticPharmaceutical ScienceCoffeamedicine.disease_causeAntioxidantsAnalytical Chemistrychemistry.chemical_compound0302 clinical medicineDrug Discoveryoxidative stressFood sciencenutricosmeticCellular SenescenceRoastingChemistryOxidantsChemistry (miscellaneous)030220 oncology & carcinogenesisMolecular Medicinecoffee silverskincoffee silverskin; oxidative stress; UVC radiation; chlorogenic acid; skin health; accelerated aging; nutricosmetic; dermaceuticskin healthCell SurvivalUltraviolet Rayschlorogenic acidOxidative phosphorylationArticlelcsh:QD241-441UVC radiation03 medical and health scienceslcsh:Organic chemistryChlorogenic acidCell Line Tumorparasitic diseasesmedicineaccelerated agingAnimalsHumansPhenolsPhysical and Theoretical ChemistryCaenorhabditis elegansPlant Extractsbusiness.industryOrganic ChemistryAccelerated agingBiotechnologyOxidative StressHaCaT030104 developmental biologyReactive Oxygen SpeciesbusinessBiomarkersOxidative stress
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Cellular Senescence and Inflammaging in Age-Related Diseases

2018

0301 basic medicineAgingArticle SubjectImmunologyCellular senescenceCell BiologyBiologymedicine.disease_causeBioinformatics03 medical and health sciencesOxidative Stress030104 developmental biologyEditorialAge relatedmedicinelcsh:PathologyAnimalsHumansSettore MED/05 - Patologia ClinicaCellular Senescence Inflammaging Age-Related DiseasesOxidative stressCellular Senescencelcsh:RB1-214Mediators of Inflammation
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From lymphopoiesis to plasma cells differentiation, the age-related modifications of B cell compartment are influenced by “inflamm-ageing”

2017

Ageing is a complex process characterized by a general decline in physiological functions with increasing morbidity and mortality. The most important aspect of ageing is the chronic inflammatory status, named “inflamm-ageing”, strictly associated with the deterioration of the immune function, termed “immunosenescence”. Both are causes of increased susceptibility of elderly to infectious diseases, cancer, dementia, cardiovascular diseases and autoimmunity, and of a decreased response to vaccination. It has been widely demonstrated that ageing has a strong impact on the remodelling of the B cell branch of immune system. The first evident effect is the significant decrease in circulati…

0301 basic medicineAgingImmunosenescenceHealth StatusPlasma CellsNaive B cellAutoimmunityInflammationBiologyLymphocyte ActivationBiochemistry03 medical and health sciences0302 clinical medicineImmune systemAntigenAge-related diseasemedicineAnimalsHumansLymphopoiesisProgenitor cellMolecular BiologyCellular SenescenceB cellInflammationB cellB-LymphocytesLymphopoiesisCell DifferentiationImmunosenescenceInflamm-ageing030104 developmental biologymedicine.anatomical_structureNeurologyImmune SystemImmunologyInflammation Mediatorsmedicine.symptomExhausted/Senescent cell030215 immunologyBiotechnologyAgeing Research Reviews
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Acute telomerase components depletion triggers oxidative stress as an early event previous to telomeric shortening

2018

Loss of function of dyskerin (DKC1), NOP10 and TIN2 are responsible for different inheritance patterns of Dyskeratosis congenita (DC; ORPHA1775). They are key components of telomerase (DKC1 and NOP10) and shelterin (TIN2), and play an important role in telomere homeostasis. They participate in several fundamental cellular processes by contributing to Dyskeratosis congenita through mechanisms that are not fully understood. Presence of oxidative stress was postulated to result from telomerase ablation. However, the resulting disturbed redox status can promote telomere attrition by generating a vicious circle, which promotes cellular senescence. This fact prompted us to study if acute loss of …

0301 basic medicineAgingTelomeraseTelomere-Binding ProteinsClinical BiochemistryCell Cycle ProteinsBiologymedicine.disease_causeBiochemistryDyskeratosis CongenitaDyskerin03 medical and health sciencesTelomere HomeostasisRibonucleoproteins Small NucleolarmedicineHumanslcsh:QH301-705.5TelomeraseCellular SenescenceTelomere ShorteningRibonucleoproteinlcsh:R5-920TelomeropathiesOrganic ChemistryNuclear ProteinsShelterinmedicine.diseaseMolecular biologyTelomereCell biologyOxidative Stress030104 developmental biologylcsh:Biology (General)DNA damageRNA InterferenceAntioxidantlcsh:Medicine (General)Oxidative stressDyskeratosis congenitaResearch PaperHeLa CellsRedox Biology
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Endothelial progenitor cells in ageing

2016

“The senescence status of somatic stem/progenitor cells contributes to ageing process”, and “an individual is as old as old are its stem cells”. These quotes represent the concepts, which are actually object of investigations of researchers involved in ageing studies.

0301 basic medicineAgingbusiness.industryCellular senescenceCell biologyEndothelial stem cell03 medical and health sciences030104 developmental biologyVasculogenesisAgeingMedicineAnimalsHumansSettore MED/05 - Patologia ClinicaProgenitor cellbusinessCellular SenescenceDevelopmental BiologyEndothelial Progenitor CellsEndothelial progenitor cells ageing
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Longevity: Lesson from model organisms

2019

Research on longevity and healthy aging promises to increase our lifespan and decrease the burden of degenerative diseases with important social and economic effects. Many aging theories have been proposed, and important aging pathways have been discovered. Model organisms have had a crucial role in this process because of their short lifespan, cheap maintenance, and manipulation possibilities. Yeasts, worms, fruit flies, or mammalian models such as mice, monkeys, and recently, dogs, have helped shed light on aging processes. Genes and molecular mechanisms that were found to be critical in simple eukaryotic cells and species have been confirmed in humans mainly by the functional analysis of…

0301 basic medicineAginglcsh:QH426-470Settore MED/06 - Oncologia Medicamedia_common.quotation_subjectved/biology.organism_classification_rank.speciesLongevityReviewBiologySignal transductionSettore MED/08 - Anatomia PatologicaModels Biologicalmodel systems03 medical and health sciences0302 clinical medicineModel systemYeastsGeneticsAnimalsHumansHealthy agingSettore MED/49 - Scienze Tecniche Dietetiche ApplicateModel organismGeneGenetics (clinical)Cellular Senescencemedia_commonMammalsved/biologyLongevityEukaryotalcsh:GeneticsSettore MED/18 - Chirurgia Generale030104 developmental biologyEvolutionary biologyHuman longevityModels AnimalDrosophilaMolecular senescence030217 neurology & neurosurgeryBiomarkers
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The Role of Osteoprotegerin and Its Ligands in Vascular Function

2019

International audience; The superfamily of tumor necrosis factor (TNF) receptors includes osteoprotegerin (OPG) and its ligands, which are receptor activators of nuclear factor kappa-B ligand (RANKL) and TNF-related apoptosis-inducing ligand (TRAIL). The OPG/RANKL/RANK system plays an active role in pathological angiogenesis and inflammation as well as cell survival. It has been demonstrated that there is crosstalk between endothelial cells and osteoblasts during osteogenesis, thus establishing a connection between angiogenesis and osteogenesis. This OPG/RANKL/RANK/TRAIL system acts on specific cell surface receptors, which are then able to transmit their signals to other intracellular comp…

0301 basic medicineAngiogenesismedicine.medical_treatmentReview030204 cardiovascular system & hematologyLigandslcsh:ChemistryTNF-Related Apoptosis-Inducing Ligand0302 clinical medicineReceptorlcsh:QH301-705.5Cellular SenescenceSpectroscopyReceptor Activator of Nuclear Factor-kappa BbiologyChemistryvascular diseaseGeneral MedicineComputer Science ApplicationsProtein Transportmedicine.anatomical_structureCytokineRANKLTumor necrosis factor alphaDisease Susceptibilitymedicine.symptomProtein BindingSignal Transductionmusculoskeletal diseasesProteasome Endopeptidase ComplexEndotheliumendotheliumNeovascularization PhysiologicInflammationCatalysisInorganic ChemistryStructure-Activity Relationship03 medical and health sciencesOsteoprotegerin[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemmedicineAnimalsHumansPhysical and Theoretical ChemistryMolecular BiologyMyocardiumRANK LigandOrganic ChemistryEndothelial Cells030104 developmental biologylcsh:Biology (General)lcsh:QD1-999osteoprotegerinOPG/RANKL/RANKCancer researchbiology.proteinBlood VesselsBiomarkers
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Targeting the chromosomal passenger complex subunit INCENP induces polyploidization, apoptosis and senescence in neuroblastoma

2019

Abstract Chromosomal passenger complex (CPC) has been demonstrated to be a potential target of cancer therapy by inhibiting Aurora B or survivin in different types of cancer including neuroblastoma. However, chemical inhibition of either Aurora B or survivin does not target CPC specifically due to off-target effects or CPC-independent activities of these two components. In a previous chromatin-focused siRNA screen, we found that neuroblastoma cells were particularly vulnerable to loss of INCENP, a gene encoding a key scaffolding component of the CPC. In this study, INCENP was highly expressed by neuroblastoma cells, and its expression decreased following retinoic acid–induced neuroblastoma …

0301 basic medicineCancer ResearchINCENP/CPC/Polyploidy/DNA damage/Apoptosis/SenescenceCarcinogenesisChromosomal Proteins Non-HistoneAurora B kinaseApoptosisBiologymedicine.disease_causeArticlePolyploidy03 medical and health sciencesMiceNeuroblastoma0302 clinical medicineNeuroblastomaSurvivinmedicineGene silencingAnimalsHumansneoplasmsCellular SenescenceINCENPmedicine.disease030104 developmental biologyOncologyApoptosisTumor progression030220 oncology & carcinogenesisCancer researchHeterograftsCarcinogenesis
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Doxorubicin anti-tumor mechanisms include Hsp60 post-translational modifications leading to the Hsp60/p53 complex dissociation and instauration of re…

2017

Hsp60 is a pro-carcinogenic chaperonin in certain tumor types by interfering with apoptosis and with tumor cell death. In these tumors, it is not known whether or not doxorubicin anti-tumor effects include a blockage of the pro-carcinogenic action of this protein. We used the human lung mucoepidermoid cell line NCI-H292 and different doses of doxorubicin to measure cell viability, cell cycle progression, cell senescence indicators, Hsp60 levels and its post-translational modifications as well as the release of the chaperonin into the extracellular environment. Cell viability was reduced in relation to doxorubicin dose and this was paralleled by the appearance of cell senescence markers. Con…

0301 basic medicineCancer ResearchLung NeoplasmsChaperoninsCellApoptosismedicine.disease_causeHistones0302 clinical medicineCellular SenescenceAntibiotics AntineoplasticAcetylationG2 Phase Cell Cycle Checkpointsmedicine.anatomical_structureOncology030220 oncology & carcinogenesisCell agingIntracellularProtein BindingSignal TransductionSenescenceCyclin-Dependent Kinase Inhibitor p21animal structuresCell Survivalchemical and pharmacologic phenomenaBiologycomplex mixturesMitochondrial ProteinsDoxorubicin Hsp60 Acetylation Ubiquitination p53 Replicative senescence03 medical and health sciencesDoxorubicin; Hsp60; p53; replicative senescence; post-translational modificationsCell Line TumormedicineHumansCell Proliferationdoxorubicin p53 Hsp60Dose-Response Relationship DrugCell growthfungiUbiquitinationChaperonin 60Molecular biology030104 developmental biologyAcetylationApoptosisDoxorubicinProteolysisCancer researchCarcinoma MucoepidermoidTumor Suppressor Protein p53CarcinogenesisProtein Processing Post-Translational
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Roles of TP53 in determining therapeutic sensitivity, growth, cellular senescence, invasion and metastasis.

2016

TP53 is a critical tumor suppressor gene that regulates cell cycle progression, apoptosis, cellular senescence and many other properties critical for control of normal cellular growth and death. Due to the pleiotropic effects that TP53 has on gene expression and cellular physiology, mutations at this tumor suppressor gene result in diverse physiological effects. T53 mutations are frequently detected in numerous cancers. The expression of TP53 can be induced by various agents used to treat cancer patients such as chemotherapeutic drugs and ionizing radiation. Radiation will induce Ataxia telangiectasia mutated (ATM) and other kinases that results in the phosphorylation and activation of TP53…

0301 basic medicineCancer Researchendocrine system diseasesMetastasimedicine.disease_causeMetastasisAntineoplastic AgentInvasionNeoplasmsTP53Neoplasm Metastasisbcl-2-Associated X ProteinAza CompoundProto-Oncogene ProteinApoptosis Regulatory ProteinbiologyCell CyclemiRMicroRNACell cycleCell biologyNeoplasm MetastasiGene Expression Regulation NeoplasticNutlin-3 chemosensitivityMdm2Molecular MedicineHumanSignal TransductionCyclin-Dependent Kinase Inhibitor p21Tumor suppressor genemiRsAntineoplastic AgentsCellular senescenceTP53; miRs; MDM2; Nutlin-3 chemosensitivity; Cellular senescence ; Invasion; Metastasis03 medical and health sciencesBcl-2-associated X proteinGeneticMDM2Proto-Oncogene ProteinsmicroRNAGeneticsmedicineHumansNeoplasm InvasivenessneoplasmsMolecular BiologyCell ProliferationNeoplasm InvasiveneAza CompoundsOncomirBridged Bicyclo Compounds HeterocyclicMicroRNAs030104 developmental biologyTumor progressionbiology.proteinNeoplasmTumor Suppressor Protein p53CarcinogenesisApoptosis Regulatory Proteins
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