Search results for "cellular senescence"

showing 10 items of 109 documents

Ovarian senescence increases liver fibrosis in humans and zebrafish with steatosis

2015

ABSTRACT Contrasting data exist on the effect of gender and menopause on the susceptibility, development and liver damage progression in non-alcoholic fatty liver disease (NAFLD). Our aim was to assess whether menopause is associated with the severity of liver fibrosis in individuals with NAFLD and to explore the issue of ovarian senescence in experimental liver steatosis in zebrafish. In 244 females and age-matched males with biopsy-proven NAFLD, we assessed anthropometric, biochemical and metabolic features, including menopausal status (self-reported); liver biopsy was scored according to ‘The Pathology Committee of the NASH Clinical Research Network’. Young and old male and female zebraf…

Liver CirrhosisMaleFibrosiBiopsyPhysiologylcsh:MedicineMedicine (miscellaneous)Body Mass IndexCohort StudiesImmunology and Microbiology (miscellaneous)FibrosisNon-alcoholic Fatty Liver DiseaseRisk FactorsOdds RatioZebrafishCellular Senescencemedicine.diagnostic_testAnthropometryFatty liverMiddle AgedOvarian senescenceMenopauseLiver biopsyModels AnimalDisease ProgressionFemaleMenopauselcsh:RB1-214Research ArticleSenescenceAdultmedicine.medical_specialtyFibrosis Menopause Non-alcoholic fatty liver disease Ovarian senescence ZebrafishNeuroscience (miscellaneous)Fibrosis; Menopause; Non-alcoholic fatty liver disease; Ovarian senescence; Zebrafish; Biochemistry Genetics and Molecular Biology (all); Medicine (miscellaneous); Immunology and Microbiology (miscellaneous); Neuroscience (miscellaneous)BiologyReal-Time Polymerase Chain ReactionGeneral Biochemistry Genetics and Molecular BiologyInternal medicinemedicinelcsh:PathologyAnimalsHumansAgedBiochemistry Genetics and Molecular Biology (all)lcsh:RSettore MED/09 - MEDICINA INTERNAOvaryOdds ratiomedicine.diseaseFibrosisEndocrinologySteatosisBody mass indexDisease Models & Mechanisms
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Calorie Restriction in Adulthood Reduces Hepatic Disorders Induced by Transient Postnatal Overfeeding in Mice

2019

International audience; Impaired early nutrition influences the risk of developing metabolic disorders in later life. We observed that transient postnatal overfeeding (OF) in mice induces long-term hepatic alterations, characterized by microsteatosis, fibrosis associated with oxidative stress (OS), and stress-induced premature senescence (SIPS). In this study, we investigated whether such changes can be reversed by moderate calorie restriction (CR). C57BL/6 male mice pups were maintained during lactation in litters adjusted to nine pups in the normal feeding (NF) group and three pups in the transient postnatal OF group. At six months of age, adult mice from the NF and OF groups were randoml…

Male0301 basic medicineStress-induced premature senescencemedicine.disease_causeMicechemistry.chemical_compound0302 clinical medicineFibrosisLactationoxidative stressCellular Senescence2. Zero hungerNutrition and DieteticsbiologySuperoxideLiver DiseasesDOHaDCatalasemedicine.anatomical_structure030220 oncology & carcinogenesisstress-induced premature senescenceFemalelcsh:Nutrition. Foods and food supplymedicine.medical_specialtyAnimals; Animals Newborn; Caloric Restriction/methods; Catalase/metabolism; Cellular Senescence; Feeding Methods/adverse effects; Female; Liver/metabolism; Liver Diseases/diet therapy; Liver Diseases/etiology; Liver Diseases/physiopathology; Male; Mice; Mice Inbred C57BL; Oxidative Stress; Superoxide Dismutase/metabolism; DOHaD; developmental programming; liver; oxidative stress; reversibility; stress-induced premature senescenceCalorie restrictionlcsh:TX341-641liverArticleLipofuscinFeeding MethodsSuperoxide dismutase03 medical and health sciencesreversibility[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemdevelopmental programmingInternal medicinemedicineAnimalsCaloric RestrictionSuperoxide Dismutasebusiness.industrymedicine.diseaseMice Inbred C57BL030104 developmental biologyEndocrinologyAnimals Newbornchemistrybiology.proteinbusinessOxidative stressFood Science
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Is the Mean Blood Leukocyte Telomere Length a Predictor for Sporadic Thoracic Aortic Aneurysm? Data from a Preliminary Study

2012

Telomeres have been postulated as a universal clock that shortens in parallel with cellular aging. They are specialized DNA-protein structures at the ends of chromosome with remarkable functions--preventing their recognition as double-stranded DNA breaks, protecting their recombination and degradation, and avoiding a DNA damage cellular response. Telomere shortening is currently considered the best aging marker, but is also a predictor for age-related diseases, including cardiovascular diseases. Biological age clearly seems to be a better predictor of vascular risk rather than chronological age. This concept is supported by key assumptions that peripheral blood leukocyte telomere content ac…

MaleAgingPathologymedicine.medical_specialtyThoracicBiological ageVascular riskBiologyBioinformaticsThoracic aortic aneurysmGeneticLeukocytesmedicineHumansSettore MED/05 - Patologia ClinicaAged; Aging; Aortic Aneurysm Thoracic; Case-Control Studies; Cellular Senescence; DNA; DNA Damage; Female; Humans; Leukocytes; Male; Middle Aged; Recombination Genetic; Telomere; Vascular DiseasesVascular DiseasesCellular Senescencevascular ageingAgedRecombination GenetictelomereAortic Aneurysm ThoracicVascular diseaseChromosomeSettore MED/23 - Chirurgia CardiacaDNAMiddle Agedmedicine.diseaseRecombinationPeripheral bloodAortic AneurysmTAATelomereCellular AgingCase-Control StudiesFemaleGeriatrics and GerontologyDNA DamageRejuvenation Research
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Sustained telomere erosion due to increased stem cell turnover during triple autologous hematopoietic stem cell transplantation.

2007

Telomeres cap chromosomal ends and are shortened throughout a lifetime. Additional telomere erosion has been documented during conventional chemotherapy or hematopoietic stem cell transplantation. Previous studies of stem cell transplantation reported variable amounts of telomere shortening with inconsistent results regarding the persistence of telomere shortening. Here we have prospectively studied telomere length and proliferation kinetics of hematopoietic cells in aggressive non-Hodgkin lymphoma patients who underwent a four-course high-dose chemotherapy protocol combined with triple autologous stem cell transplantation. We observed sustained telomere shortening in hematopoietic cells af…

MaleCancer ResearchTransplantation Conditioningmedicine.medical_treatmentHematopoietic stem cell transplantationAntibodies Monoclonal Murine-DerivedAutologous stem-cell transplantationAntineoplastic Combined Chemotherapy ProtocolsGranulocyte Colony-Stimulating FactorLymphocytesProspective StudiesCellular SenescenceEtoposideMyelopoiesisLymphoma Non-HodgkinAntibodies MonoclonalHematologyMiddle AgedTelomereCombined Modality TherapyHaematopoiesisVincristineFemaleStem cellRituximabCell DivisionPrednisoloneTransplantation AutologousDrug Administration ScheduleGeneticsmedicineHumansMolecular BiologyCyclophosphamideChemotherapyPeripheral Blood Stem Cell Transplantationbusiness.industryCell BiologyMyeloablative Agonistsmedicine.diseaseHematopoietic Stem CellsTelomereLymphomaTransplantationClinical Trials Phase III as TopicDoxorubicinImmunologyCancer researchbusinessGranulocytesExperimental hematology
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Roles of the Raf/MEK/ERK and PI3K/PTEN/Akt/mtor pathways in controlling growth and sensitivity to therapy-implications for cancer and aging

2011

Dysregulated signaling through the Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways is often the result of genetic alterations in critical components in these pathways or upstream activators. Unrestricted cellular proliferation and decreased sensitivity to apoptotic-inducing agents are typically associated with activation of these pro-survival pathways. This review discusses the functions these pathways have in normal and neoplastic tissue growth and how they contribute to resistance to apoptotic stimuli. Crosstalk and commonly identified mutations that occur within these pathways that contribute to abnormal activation and cancer growth will also be addressed. Finally the recently described …

MaleMAPK/ERK pathwayAgingMAP Kinase Signaling SystemCancer aging RAF MEK mTORApoptosisReviewBiologyPI3KModels BiologicalApoptosis; Cancer; Kinases; MEK; MTOR; PI3K; Protein phosphorylation; RAF; Signal transductionMicePhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineCancer stem cellNeoplasmscancerAnimalsHumansPTENProtein kinase BCellular SenescencePI3K/AKT/mTOR pathwayCell Proliferation030304 developmental biology0303 health sciencesKinaseTOR Serine-Threonine KinasesapoptosisPTEN PhosphohydrolaseRafCell BiologyMEKprotein phosphorylation3. Good healthCell biologyCrosstalk (biology)kinases030220 oncology & carcinogenesisMutationmTORCancer researchbiology.proteinFemaleraf KinasesProto-Oncogene Proteins c-aktCell agingsignal transduction
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Quiescence Modulates Stem Cell Maintenance and Regenerative Capacity in the Aging Brain.

2018

The function of somatic stem cells declines with age. Understanding the molecular underpinnings of this decline is key to counteract age-related disease. Here, we report a dramatic drop in the neural stem cells (NSCs) number in the aging murine brain. We find that this smaller stem cell reservoir is protected from full depletion by an increase in quiescence that makes old NSCs more resistant to regenerate the injured brain. Once activated, however, young and old NSCs show similar proliferation and differentiation capacity. Single-cell transcriptomics of NSCs indicate that aging changes NSCs minimally. In the aging brain, niche-derived inflammatory signals and the Wnt antagonist sFRP5 induce…

MaleNeurogenesisSubventricular zoneInflammationBiologyGeneral Biochemistry Genetics and Molecular BiologyTranscriptome03 medical and health sciencesMice0302 clinical medicineNeural Stem CellsmedicineAging brainsFRP5stem cell agingAnimalsHomeostasisquiescenceStem Cell Nichereproductive and urinary physiologyCellular Senescence030304 developmental biologyneural stem cellsCell Proliferation0303 health sciencesWnt signaling pathwayAge Factorssubventricular zoneBrainmodelingCell DifferentiationinterferonWnt signalingNeural stem cellCell biologynervous system diseasesNerve RegenerationMice Inbred C57BLmedicine.anatomical_structurenervous systeminflammationsimulationsmedicine.symptomStem cellbiological phenomena cell phenomena and immunitysingle-cell transcriptomics030217 neurology & neurosurgeryCell DivisionAdult stem cellCell
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Consequences on offspring of abnormal function in ageing gametes.

2000

The present review aims to analyse (i) the molecular, biochemical and cellular changes that accompany oocyte and sperm ageing in any of the internal or external environments where they can reside, and (ii) the consequences of the abnormal function in ageing gametes on pre- and post-implantation development and later life of offspring. This review also aims to propose and discuss cellular/molecular mechanisms framed within the 'free radical theory of ageing'. It appears that the ageing of gametes prior to fertilization may affect many molecular, biochemical and cellular pathways that may jeopardize not only pre- and post-implantation embryo/fetal development but also later life of offspring.…

MaleOffspringmedia_common.quotation_subjectBiologyAntioxidantsAndrologyPregnancymedicineAnimalsHumansCellular Senescencemedia_commonGeneticsPregnancyReproductive successLongevityPregnancy OutcomeObstetrics and GynecologyEmbryomedicine.diseaseSpermSpermatozoaOxidative Stressmedicine.anatomical_structureReproductive MedicineAgeingOocytesGameteFemaleReactive Oxygen SpeciesHuman reproduction update
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Intrinsically determined cell death of developing cortical interneurons.

2009

The cell death of inhibitory neurons, which originate far from the cortical areas to which they migrate during embryonic development, is determined autonomously rather than by competition for trophic signals from other cell types. It has long been known that apoptosis, a form of programmed cell death, eliminates young cells from developing tissues. In the field of neurobiology, it is widely believed that developmental neuronal-cell death results from cellular competition for environmentally derived survival signals that selects for an optimally sized and properly wired population of neurons. This study of developmental cell death in the mouse cortex in vivo, in vitro and after transplantati…

MaleProgrammed cell deathInterneurongenetic structuresCell SurvivalPopulationApoptosisCell CountNeocortexBiologyArticle03 medical and health sciencesMice0302 clinical medicineNeural Stem CellsInterneuronsmedicineAnimalseducationCellular Senescence030304 developmental biologybcl-2-Associated X Protein0303 health scienceseducation.field_of_studyMultidisciplinaryNeocortexMembrane GlycoproteinsCaspase 3musculoskeletal neural and ocular physiologyPyramidal CellsfungiProtein-Tyrosine KinasesCell biologyTransplantationMice Inbred C57BLmedicine.anatomical_structurenervous systemAnimals NewbornInhibitory Postsynaptic PotentialsCerebral cortexbiology.proteinFemaleCell aging030217 neurology & neurosurgeryNeurotrophinNature
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Functional characterization of the dural sinuses as a neuroimmune interface

2021

Summary Despite the established dogma of central nervous system (CNS) immune privilege, neuroimmune interactions play an active role in diverse neurological disorders. However, the precise mechanisms underlying CNS immune surveillance remain elusive; particularly, the anatomical sites where peripheral adaptive immunity can sample CNS-derived antigens and the cellular and molecular mediators orchestrating this surveillance. Here, we demonstrate that CNS-derived antigens in the cerebrospinal fluid (CSF) accumulate around the dural sinuses, are captured by local antigen-presenting cells, and are presented to patrolling T cells. This surveillance is enabled by endothelial and mural cells formin…

MaleT-LymphocytesDura materCentral nervous systemAntigen-Presenting CellsCranial SinusesBiologyGeneral Biochemistry Genetics and Molecular BiologyMural cell03 medical and health sciences0302 clinical medicineImmune privilegemedicineAnimalsHomeostasisHumansAntigensCellular Senescence030304 developmental biologyAntigen Presentation0303 health sciencesMultiple sclerosisImmunityMeningesmedicine.diseaseAcquired immune systemResearch HighlightChemokine CXCL12Mice Inbred C57BLPhenotypeNeuroimmunologymedicine.anatomical_structureFemaleDura MaterStromal CellsNeuroscience030217 neurology & neurosurgeryCell
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Physiology of the aging bone and mechanisms of action of bisphosphonates.

2011

Fragility fractures, a major public health concern, are expected to further increase due to aging of the world populations because age remains a cardinal, independent determinant of fracture risk. With aging the balance between bone formation and resorption during the remodeling process becomes negative, with increased resorption and reduced formation. Bisphosphonates (BPs) are widely prescribed anti-resorptive agents that inhibit osteoclasts attachment to bone matrix and enhance osteoclast apoptosis. BPs can be divided into nitrogen-containing (N-BPs) and non-nitrogen-containing BPs (non-N-BPs). Both classes induce apoptosis but they evoke it differently. Several studies have examined the …

Malemedicine.medical_specialtyAgingSettore MED/09 - Medicina Internamedicine.medical_treatmentOsteoporosisurologic and male genital diseasesBone resorptionBone and BonesBone remodelingOsteoclastInternal medicinemedicineHumansCellular SenescenceBONE BONE TURNOVER FRAGILITY FRACTURES AGING BISPHOSPHONATESOsteoblastsBone Density Conservation AgentsDiphosphonatesbusiness.industryBone metastasisOsteoblastBisphosphonatemedicine.diseaseEndocrinologymedicine.anatomical_structureOsteocyteFemaleBone RemodelingGeriatrics and GerontologybusinessGerontologyhormones hormone substitutes and hormone antagonistsBiogerontology
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