Integrating environment-by-epigenome interactions into a tractable model of epigenetic aging
将环境与表观基因组的相互作用整合到易于处理的表观遗传衰老模型中
基本信息
- 批准号:10674255
- 负责人:
- 金额:$ 27.34万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2022
- 资助国家:美国
- 起止时间:2022-09-02 至 2024-08-31
- 项目状态:已结题
- 来源:
- 关键词:AcuteAddressAffectAgeAgingAirAutomobile DrivingBiologicalBiological AgingBiological MarkersBiological ProcessChronicChronologyClimateClinical ResearchCommunitiesComplexDNADevelopmentDisastersDiseaseDoseDose-RateElderlyEnvironmentEnvironmental ExposureEnvironmental PollutionEnvironmental Risk FactorEpigenetic ProcessEventExposure toFacility DesignsFishesGeneticGenomeGenomicsGoalsHealthHeart DiseasesIndividualIonizing radiationJapanese KillifishLifeLife Cycle StagesLinkLongevityMalignant NeoplasmsMeasuresMediatingMedicalMethylationModelingMolecularNatureNuclear AccidentsNuclear EnergyNuclear WarfareNucleotidesOccupational ExposureOryziinaeOutcomePatternPerformancePhysiologicalPhysiologyPlayProcessPublic HealthRadiationRadiation AccidentsRadiation exposureRecording of previous eventsRegimenReproductive HealthResolutionResourcesRiskRiversRoleShapesSiteSocial EnvironmentTerrorismTestingTimeToxicologyTravelWorkage relatedaquatic organismbasecombinatorialdensitydesigndirty bombdisorder riskepigenomeexperienceirradiationlife historymethylomemiddle agemortalitynovelprogramsradiation riskresponsesocialstemstressortheories
项目摘要
Project Summary
The goal of the project is to discover how the environment interacts with epigenetic aging processes to affect
biological aging. Risk of radiation exposure occurring through occupational exposures, medical therapies, or
environmental disasters involving ionizing radiation (IR), either due to nuclear accidents, nuclear warfare,
and/or terrorist attacks (e.g., attacks on nuclear energy facilities, dirty bombs) are acutely relevant to
contemporary public health. However, health impacts resulting from such exposures are difficult to predict due
to variable dose rates, duration of exposure, age-specific effects, and the environmental and social context of
exposure. Although testing the outcome of each combinatorial scenario isn’t feasible, a fundamental
understanding of how environmental and age-dependent variables interact with IR exposure can be achieved
through approaches that incorporate environmental complexity and realistic dosing regimens.
Recent advances demonstrate a role for the epigenome in biological aging as it provides a molecular context
for integrating both genetic and environmental influences into aging programs. Epigenetic clocks summarize
the readout of age associated hyper- and hypo-methylation from a selection of loci across the genome which
are collectively capable of predicting chronological age with high accuracy. Despite their unprecedented
accuracy, the age indicated by epigenetic clocks can differ from an individual’s actual age. The magnitude and
directionality of this epigenetic-to-chronological age mismatch is associated with physiological function and
disease risk. For example, advanced epigenetic age relative to their chronological age is associated with
cancer, heart disease, and all-cause mortality. The underlying causes of epigenetic-to-chronological age
discordance are not resolved but both genetic and environmental factors appear to play a role. To empirically
address causal relationships between environmental conditions and epigenetic aging, this project will take
advantage of recently developed epigenetic clocks for the experimentally and genetically tractable medaka fish
(Oryzias latipes) model.
The work encompasses three primary objectives: (1) Test the hypothesis that chronic exposure to
environmentally relevant doses of ionizing radiation accelerate and shape epigenetic aging trajectories. (2)
Determine how an individual’s developmental exposure history interacts with subsequent radiation exposure to
affect biological aging trajectories. (3) Identify windows of vulnerability occurring across the lifespan in which
environmental exposures disproportionately impacts epigenetic aging trajectories. Together, this work will
advance a life course and toxicological understanding of how environmental challenges associated with
radiological disaster events shape biological aging and attendant organismal physiology.
项目总结
项目成果
期刊论文数量(2)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
The rate of epigenetic drift scales with maximum lifespan across mammals.
- DOI:10.1038/s41467-023-43417-6
- 发表时间:2023-11-25
- 期刊:
- 影响因子:16.6
- 作者:Bertucci-Richter, Emily M.;Parrott, Benjamin B.
- 通讯作者:Parrott, Benjamin B.
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Benjamin Barrow Parrott其他文献
Benjamin Barrow Parrott的其他文献
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