2024
Targeting CDK2 to circumvent treatment resistance in HR+ breast cancer
Arrizabalaga L, García-Torralba E, Galluzzi L, Buqué A. Targeting CDK2 to circumvent treatment resistance in HR+ breast cancer. Trends In Molecular Medicine 2024 PMID: 39732571, DOI: 10.1016/j.molmed.2024.12.009.Peer-Reviewed Original ResearchSenNet recommendations for detecting senescent cells in different tissues
Suryadevara V, Hudgins A, Rajesh A, Pappalardo A, Karpova A, Dey A, Hertzel A, Agudelo A, Rocha A, Soygur B, Schilling B, Carver C, Aguayo-Mazzucato C, Baker D, Bernlohr D, Jurk D, Mangarova D, Quardokus E, Enninga E, Schmidt E, Chen F, Duncan F, Cambuli F, Kaur G, Kuchel G, Lee G, Daldrup-Link H, Martini H, Phatnani H, Al-Naggar I, Rahman I, Nie J, Passos J, Silverstein J, Campisi J, Wang J, Iwasaki K, Barbosa K, Metis K, Nernekli K, Niedernhofer L, Ding L, Wang L, Adams L, Ruiyang L, Doolittle M, Teneche M, Schafer M, Xu M, Hajipour M, Boroumand M, Basisty N, Sloan N, Slavov N, Kuksenko O, Robson P, Gomez P, Vasilikos P, Adams P, Carapeto P, Zhu Q, Ramasamy R, Perez-Lorenzo R, Fan R, Dong R, Montgomery R, Shaikh S, Vickovic S, Yin S, Kang S, Suvakov S, Khosla S, Garovic V, Menon V, Xu Y, Song Y, Suh Y, Dou Z, Neretti N. SenNet recommendations for detecting senescent cells in different tissues. Nature Reviews Molecular Cell Biology 2024, 25: 1001-1023. PMID: 38831121, PMCID: PMC11578798, DOI: 10.1038/s41580-024-00738-8.Peer-Reviewed Original ResearchSenescent cellsDetect senescent cellsIrreversible cell cycle arrestCellular senescenceCell cycle arrestSenescence markersBiomarker Working GroupCycle arrestCellular senescence markersBiological processesCell biologyPostmitotic cellsSenescent phenotypeCirculating markersTissue culture studiesSenescence signatureSenescenceCellsMorphological featuresDetrimental roleTissueMarkersSeasonal investigationCellular Dynamics of Fas-Associated Death Domain in the Regulation of Cancer and Inflammation
Ranjan K, Pathak C. Cellular Dynamics of Fas-Associated Death Domain in the Regulation of Cancer and Inflammation. International Journal Of Molecular Sciences 2024, 25: 3228. PMID: 38542202, PMCID: PMC10970579, DOI: 10.3390/ijms25063228.Peer-Reviewed Original ResearchConceptsFas-associated death domainDeath domainDeath receptorsInitiation of apoptotic signalingRegulate programmed cell deathExpression of Fas-associated death domainSignaling pathwayCellular dynamicsRegulator of inflammatory signalingRegulation of cancerAdaptor proteinActivated caspasesApoptotic functionApoptosis signalingSubcellular localizationApoptotic signalingCellular homeostasisCell deathCell survivalCoordinated removalCellular senescenceIntracellular expressionCell proliferationSpatiotemporal mechanismsInflammatory signalingDisruption 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 oocytesGene expression meta-analysis reveals aging and cellular senescence signatures in scleroderma-associated interstitial lung disease
Yang M, Lee S, Neely J, Hinchcliff M, Wolters P, Sirota M. Gene expression meta-analysis reveals aging and cellular senescence signatures in scleroderma-associated interstitial lung disease. Frontiers In Immunology 2024, 15: 1326922. PMID: 38348044, PMCID: PMC10859856, DOI: 10.3389/fimmu.2024.1326922.Peer-Reviewed Original ResearchConceptsScleroderma-associated interstitial lung diseaseSSc-ILDInterstitial lung diseaseLung tissueGene expression meta-analysisPulmonary fibrosisLung diseaseSenescence signatureDegree of skin involvementIdiopathic pulmonary fibrosisTelomere lengthType II alveolar cellsCellular senescence signaturesCellular senescenceIndependent of ageSkin involvementSSc skinExpression meta-analysisHealthy controlsAssociated with degreeAlveolar cellsLungMeta-analysisAging genesFibrosis
2023
Differences in syncytia formation by SARS-CoV-2 variants modify host chromatin accessibility and cellular senescence via TP53
Lee J, Menasche B, Mavrikaki M, Uyemura M, Hong S, Kozlova N, Wei J, Alfajaro M, Filler R, Müller A, Saxena T, Posey R, Cheung P, Muranen T, Heng Y, Paulo J, Wilen C, Slack F. Differences in syncytia formation by SARS-CoV-2 variants modify host chromatin accessibility and cellular senescence via TP53. Cell Reports 2023, 42: 113478. PMID: 37991919, PMCID: PMC10785701, DOI: 10.1016/j.celrep.2023.113478.Peer-Reviewed Original ResearchConceptsChromatin accessibilityProteomic compositionCellular senescenceTP53 stabilizationSARS-CoV-2 spikeCell-cell fusionPathogenic coronavirusesSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variantsSenescence-associated inflammationSARS-CoV-2 infectionMiddle East respiratory syndromeAccessibility stateInflammatory cytokine releaseSevere respiratory infectionsSARS-CoV-2 variantsSignificant public health threatCoronavirus disease 2019SARS-CoV-2Public health threatBreakthrough infectionsRespiratory infectionsCytokine releaseSenescenceDisease 2019Respiratory syndromeGeroscience-Centric Perspective for Geriatric Psychiatry: Integrating Aging Biology With Geriatric Mental Health Research
Diniz B, Seitz-Holland J, Sehgal R, Kasamoto J, Higgins-Chen A, Lenze E. Geroscience-Centric Perspective for Geriatric Psychiatry: Integrating Aging Biology With Geriatric Mental Health Research. American Journal Of Geriatric Psychiatry 2023, 32: 1-16. PMID: 37845116, PMCID: PMC10841054, DOI: 10.1016/j.jagp.2023.09.014.Peer-Reviewed Original ResearchLife’s Essential 8 Optimizing Health in Older Adults
Kumar M, Orkaby A, Tighe C, Villareal D, Billingsley H, Nanna M, Kwak M, Rohant N, Patel S, Goyal P, Hummel S, Al-Malouf C, Kolimas A, Krishnaswami A, Rich M, Kirkpatrick J, Damluji A, Kuchel G, Forman D, Alexander K. Life’s Essential 8 Optimizing Health in Older Adults. JACC Advances 2023, 2: 100560. PMID: 37664644, PMCID: PMC10470487, DOI: 10.1016/j.jacadv.2023.100560.Peer-Reviewed Original ResearchClinical cardiovascular diseaseOlder adultsPrevention targetsTraditional CVD risk factorsCVD-free survivalCVD risk factorsGoals of careAmerican Heart AssociationQuality of lifeGeriatric syndromesHeart AssociationRisk factorsCardiovascular diseaseHigh prevalenceCell exhaustionChronologic ageSleep healthOlder individualsMitochondrial dysfunctionStem cell exhaustionResult of advancesCellular senescenceAdultsPublic healthIntercellular communication
2022
Cellular senescence is immunogenic and promotes anti-tumor immunity
Marin I, Boix O, Garcia-Garijo A, Sirois I, Caballe A, Zarzuela E, Ruano I, Attolini C, Prats N, López-Domínguez J, Kovatcheva M, Garralda E, Muñoz J, Caron E, Abad M, Gros A, Pietrocola F, Serrano M. Cellular senescence is immunogenic and promotes anti-tumor immunity. Cancer Discovery 2022, 13: 410-431. PMID: 36302218, PMCID: PMC7614152, DOI: 10.1158/2159-8290.cd-22-0523.Peer-Reviewed Original ResearchConceptsCD8 T cellsAntitumor immune responseImmunogenic cell deathDendritic cellsSenescent cancer cellsT cellsCancer cellsImmune responseAntigen-specific CD8 T cellsSenescent cellsRelease of alarminsAnti-tumor immunityInnate immune cellsHuman primary cancer cellsActivation of IFNCellular senescencePrimary cancer cellsAdaptive immune systemCell deathCD8 lymphocytesAntitumor protectionImmune cellsImmune systemContext of cancerInduction of senescenceSenolytic treatment reduces cell senescence and necroptosis in Sod1 knockout mice that is associated with reduced inflammation and hepatocellular carcinoma
Thadathil N, Selvarani R, Mohammed S, Nicklas E, Tran A, Kamal M, Luo W, Brown J, Lawrence M, Borowik A, Miller B, Van Remmen H, Richardson A, Deepa S. Senolytic treatment reduces cell senescence and necroptosis in Sod1 knockout mice that is associated with reduced inflammation and hepatocellular carcinoma. Aging Cell 2022, 21: e13676. PMID: 35869934, PMCID: PMC9381894, DOI: 10.1111/acel.13676.Peer-Reviewed Original ResearchConceptsSod1KO miceHepatocellular carcinomaQ treatmentCellular senescenceSenescence-associated secretory phenotype factorsMarkers of necroptosisSod1 knockout miceChronic liver diseaseMarkers of inflammationMonths of ageExpression of p16WT levelsSenolytic treatmentLiver diseaseReduced inflammationCu/Zn-superoxide dismutaseMacrophage levelsLiver fibrosisPhenotype factorsLiver cancerNecrostatin-1sKnockout miceAge-associated pathologiesMice nullInflammationHuman Down syndrome microglia are up for a synaptic feast
Kiral FR, Park IH. Human Down syndrome microglia are up for a synaptic feast. Cell Stem Cell 2022, 29: 1007-1008. PMID: 35803219, DOI: 10.1016/j.stem.2022.06.008.Peer-Reviewed Original ResearchDifferential RNAseq Analysis of an Ex-Vivo Human Fibrotic Tissue Slice Model Reveals Dysregulated Genes of Cellular Senescence and YAP/TAZ Signaling in Fibrosis
Pineda R, Mitash N, Kohler K, Melo Narvaez M, Sembrat J, Fangping M, Lehmann M, Kaminski N, Koenigshoff M. Differential RNAseq Analysis of an Ex-Vivo Human Fibrotic Tissue Slice Model Reveals Dysregulated Genes of Cellular Senescence and YAP/TAZ Signaling in Fibrosis. 2022, a5229-a5229. DOI: 10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a5229.Peer-Reviewed Original ResearchTick tock, tick tock: Mouse culture and tissue aging captured by an epigenetic clock
Minteer C, Morselli M, Meer M, Cao J, Higgins‐Chen A, Lang SM, Pellegrini M, Yan Q, Levine ME. Tick tock, tick tock: Mouse culture and tissue aging captured by an epigenetic clock. Aging Cell 2022, 21: e13553. PMID: 35104377, PMCID: PMC8844113, DOI: 10.1111/acel.13553.Peer-Reviewed Original ResearchConceptsMouse embryonic fibroblastsDNA methylationEpigenetic agingImportant chromatin regulatorsPolycomb group (PcG) factorsAnti-aging interventionsChromatin regulatorsEmbryonic fibroblastsCellular senescenceTissue agingCellular agingEpigenetic clocksMultiple tissuesMouse tissuesCaloric restrictionMechanistic insightsAging changesKidney fibroblastsReduced representationTime pointsPhysiological agingMouse culturesSuch alterationsTick-TockTissue
2021
Peroxiredoxin 6 protects irradiated cells from oxidative stress and shapes their senescence-associated cytokine landscape
Salovska B, Kondelova A, Pimkova K, Liblova Z, Pribyl M, Fabrik I, Bartek J, Vajrychova M, Hodny Z. Peroxiredoxin 6 protects irradiated cells from oxidative stress and shapes their senescence-associated cytokine landscape. Redox Biology 2021, 49: 102212. PMID: 34923300, PMCID: PMC8688892, DOI: 10.1016/j.redox.2021.102212.Peer-Reviewed Original ResearchConceptsSenescence-associated secretory phenotypePeroxiredoxin 6Senescent cellsIrreversible cell cycle arrestProtein secretory pathwayStress-induced cell deathProteome-level changesProteome-wide analysisCyclin-dependent kinasesProtein sulfhydryl oxidationOxidative stressPeroxiredoxin family membersExtracellular matrix proteinsComplex stress responseHTERT-RPE-1Cell cycle arrestSecretory pathwayRadiation-induced senescenceRedox homeostasisCellular senescenceDependent kinasesSecretome analysisStress responseSenescent phenotypeAntioxidant proteinsNucleotide‐binding domain and leucine‐rich‐repeat‐containing protein X1 deficiency induces nicotinamide adenine dinucleotide decline, mechanistic target of rapamycin activation, and cellular senescence and accelerates aging lung‐like changes
Shin HJ, Kim S, Park H, Shin M, Kang I, Kang M. Nucleotide‐binding domain and leucine‐rich‐repeat‐containing protein X1 deficiency induces nicotinamide adenine dinucleotide decline, mechanistic target of rapamycin activation, and cellular senescence and accelerates aging lung‐like changes. Aging Cell 2021, 20: e13410. PMID: 34087956, PMCID: PMC8282248, DOI: 10.1111/acel.13410.Peer-Reviewed Original ResearchConceptsCellular senescenceActivation of mTORNucleotide-binding domainCellular senescence responseReplicative cellular senescenceNLR family membersOrganismal agingCellular physiologyMitochondrial moleculesSenescence responseCellular locationProtein X1Crucial regulatorMechanistic targetMitochondrial functionMolecular hallmarksNLRX1 functionRapamycin (mTOR) activationMitochondrial dysfunctionSenescenceMTORPharmacological inhibitionNLRX1BiologyAging LungAltered endocytosis in cellular senescence
Shin EY, Soung NK, Schwartz MA, Kim EG. Altered endocytosis in cellular senescence. Ageing Research Reviews 2021, 68: 101332. PMID: 33753287, PMCID: PMC8131247, DOI: 10.1016/j.arr.2021.101332.Peer-Reviewed Original Research
2020
Non-coding RNAs as Regulators of Cellular Senescence in Idiopathic Pulmonary Fibrosis and Chronic Obstructive Pulmonary Disease
Omote N, Sauler M. Non-coding RNAs as Regulators of Cellular Senescence in Idiopathic Pulmonary Fibrosis and Chronic Obstructive Pulmonary Disease. Frontiers In Medicine 2020, 7: 603047. PMID: 33425948, PMCID: PMC7785852, DOI: 10.3389/fmed.2020.603047.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsNon-coding RNAsCellular stress responseNon-coding RNACellular senescenceCell fateChronic obstructive pulmonary diseaseStress responseAlternative cell fatesIdiopathic pulmonary fibrosisLong non-coding RNAsObstructive pulmonary diseaseCellular stressorsCellular stressKey regulatorSenescencePulmonary diseaseDNA damagePulmonary fibrosisMitochondrial dysfunctionRNACellular mechanismsChronic lung diseasePotential therapeutic roleRegulatorOxidative stressOsteocyte RANKL is required for cortical bone loss with age and is induced by senescence
Kim HN, Xiong J, MacLeod RS, Iyer S, Fujiwara Y, Cawley KM, Han L, He Y, Thostenson JD, Ferreira E, Jilka RL, Zhou D, Almeida M, O'Brien CA. Osteocyte RANKL is required for cortical bone loss with age and is induced by senescence. JCI Insight 2020, 5: e138815. PMID: 32870816, PMCID: PMC7566701, DOI: 10.1172/jci.insight.138815.Peer-Reviewed Original ResearchConceptsCortical bone lossBone lossControl miceAged miceCortical boneAge-associated bone lossOsteoclastogenic cytokine RANKLOsteocyte-derived RANKLTrabecular boneMonths of ageSenescent cellsConditional knockout miceHuman cell culture modelsRANKL levelsCytokine RANKLRANKL productionKnockout miceTranscription factor GATA4Cell culture modelSenolytic compoundsRANKLMiceAgeBoneCellular senescenceIntegrin-mediated adhesions in regulation of cellular senescence
Shin EY, Park JH, You ST, Lee CS, Won SY, Park JJ, Kim HB, Shim J, Soung NK, Lee OJ, Schwartz MA, Kim EG. Integrin-mediated adhesions in regulation of cellular senescence. Science Advances 2020, 6: eaay3909. PMID: 32494696, PMCID: PMC7202880, DOI: 10.1126/sciadv.aay3909.Peer-Reviewed Original ResearchConceptsClathrin-mediated endocytosisCellular senescenceG protein-coupled receptor kinasesProtein-coupled receptor kinasesElevated reactive oxygen species (ROS) productionIntegrin-mediated adhesionIntegrin endocytosisAmphiphysin 1Exchange factorReactive oxygen species productionReceptor kinaseOxygen species productionMolecular mechanismsCalpain cleavageSenescenceCell adhesionDirect competitionHuman fibroblastsGIT levelsSpecies productionΒPixNew therapeutic directionIntegrinsEndocytosisCentral role
2019
A Unique SUMO-Interacting Motif of Trx2 Is Critical for Its Mitochondrial Presequence Processing and Anti-oxidant Activity
Chen C, Wang K, Zhang H, Zhou HJ, Chen Y, Min W. A Unique SUMO-Interacting Motif of Trx2 Is Critical for Its Mitochondrial Presequence Processing and Anti-oxidant Activity. Frontiers In Physiology 2019, 10: 1089. PMID: 31555141, PMCID: PMC6727865, DOI: 10.3389/fphys.2019.01089.Peer-Reviewed Original ResearchSUMO-interacting motifMitochondrial processing peptidaseReactive oxygen speciesMitochondrial intermediate peptidaseStress-induced cellular senescenceOxidative stress-induced cellular senescenceMitochondrial redox proteinsMitochondrial thioredoxin 2Excess reactive oxygen speciesMitochondrial processingPresequence processingProcessing peptidaseTrx2 proteinMitochondrial targetingMassive reactive oxygen speciesAntisenescence activityCellular senescenceThioredoxin 2Chemical inhibitionMature formRedox proteinsUnprocessed formProteinTrx2Catalytic site
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