Probing the Pathophysiology of ME/CFS through Proteomics and Metabolomics
通过蛋白质组学和代谢组学探讨 ME/CFS 的病理生理学
基本信息
- 批准号:10237224
- 负责人:
- 金额:$ 115.8万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2017
- 资助国家:美国
- 起止时间:2017-09-30 至 2023-03-31
- 项目状态:已结题
- 来源:
- 关键词:AccelerometerAffectBiochemicalBiological MarkersBiological ProcessBlood CirculationBlood PressureBlood specimenCardiopulmonaryCellsCharacteristicsChronic Fatigue SyndromeClinicalCognitiveCytokine SignalingDNADataDiseaseEtiologyExerciseExercise TestExertionExhibitsFatigueFunctional disorderGene ExpressionGrowthHeart RateHormonesImmune System DiseasesImmunoassayInflammation MediatorsInflammatoryLipidsMalaiseMeasuresMediatingMetabolicMetabolic PathwayMetabolismMitochondrial DNAMolecularMolecular ProbesNeurotransmittersOutcome MeasureOutcome StudyOxygen ConsumptionPainPathway AnalysisPathway interactionsPatientsPhysical EffortsPhysical activityPhysiologicalPlasmaPlayProductionProstaglandinsProteinsProteomicsProtocols documentationPsyche structureRNAResearchResearch PersonnelRoleSamplingSerumSignaling MoleculeSignaling ProteinSleepStressSubgroupSurveysSymptomsTimeWorkdigitaldisabling symptomexperienceextracellular vesiclesimmune activationimmunogenicinsightmetabolomemetabolomicsnovel markerprimary outcomeprotein metaboliteresponsesedentaryvesicular release
项目摘要
PROJECT SUMMARY: CLINICAL PROJECT 2: PROBING THE PATHOPHYSIOLOGY OF ME/CFS
The underlying reason for the profound fatigue, pain, cognitive difficulties, and the peculiar response to
physical effort of ME/CFS patients, is not understood. One reason that many ME/CFS patients are unable to
work is that their maximal ability to produce energy, measured by cardiopulmonary exercise testing (CPET), is
extremely low. For many ME/CFS patients an increase in physical or mental activity results in an increase in
symptoms termed post-exertional malaise. Prior work by Cornell Center investigators found that most
ME/CFS patients who undergo CPET cannot reproduce, a day later, one or more objective measures such as
oxygen consumption at maximal threshold intensities, and/or exhibit abnormalities in blood pressure and/or
heart rate response. The cause of post-exertional malaise, like the cause of ME/CFS, is not understood,
although it is one of the most debilitating symptoms of ME/CFS sufferers.
Our central hypothesis is that the study of postexertional malaise provides an exciting opportunity to
obtain new insights into the etiology of ME/CFS. We will obtain samples from patients at several different time
points, prior to an exercise challenge, when they are experiencing their usual levels of symptoms, and at a time
of heightened symptoms, post exercise, enabling deeper insight into abnormal biological functioning
associated with the disease. By analyzing, in conjunction with physiological data, metabolites, circulating
inflammatory molecules, and extracellular vesicle (EV) cargo in blood samples from before and after
exercise sessions, we aim to uncover markers and mechanisms of post-exertional malaise in ME/CFS. Our
broad survey of possible molecular responses to exercise will include inflammatory proteins and immunogenic
mitochondrial DNA (mtDNA) fragments, targeted and untargeted metabolomics of blood serum, and a detailed
proteomic and metabolomic characterization of EVs. EVs are released into the circulation during exercise and
could therefore contain biomarkers or contain cargo that plays an active role in mediating the abnormal
response to physical activity in ME/CFS. EVs cargo includes signaling proteins, lipids, hormones, and RNAs
that can influence the growth, metabolic activity, and gene expression in target cells with which they fuse.
We expect that the metabolomic analyses of serum and EVs have particularly high potential to detect
ME/CFS-specific changes in the response to exercise, because the metabolome integrates downstream
effects from almost any physiological pathway. Therefore, in addition to conventional targeted metabolomics,
we will introduce untargeted metabolomic analyses as a powerful approach toward discovery of new or
unexpected ME/CFS-associated changes in primary metabolism or the production of signaling molecules such
as hormones, prostaglandins, or neurotransmitters. As a primary outcome of this study, we expect to provide
comprehensive data on metabolomic and proteomic changes associated with post-exertional malaise in
ME/CFS that will enable identifications of novel markers and mechanisms associated with this disease.
项目概述:临床项目2:探讨me / cfs的病理生理
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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MAUREEN REBECCA HANSON其他文献
MAUREEN REBECCA HANSON的其他文献
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{{ truncateString('MAUREEN REBECCA HANSON', 18)}}的其他基金
Cornell ME/CFS Collaborative Research Center Administrative Core
康奈尔大学 ME/CFS 合作研究中心行政核心
- 批准号:
10627288 - 财政年份:2017
- 资助金额:
$ 115.8万 - 项目类别:
Cornell ME/CFS Collaborative Research Center
康奈尔大学 ME/CFS 合作研究中心
- 批准号:
10237220 - 财政年份:2017
- 资助金额:
$ 115.8万 - 项目类别:
Microbiomes and Inflammation in Chronic Fatigue Syndrome
慢性疲劳综合征中的微生物组和炎症
- 批准号:
8496710 - 财政年份:2012
- 资助金额:
$ 115.8万 - 项目类别:
Microbiomes and Inflammation in Chronic Fatigue Syndrome
慢性疲劳综合征中的微生物组和炎症
- 批准号:
8359145 - 财政年份:2012
- 资助金额:
$ 115.8万 - 项目类别:
The Relationship of XMRV to Functional Status and Co-infections in Chronic Fatigu
XMRV 与慢性疲劳功能状态和合并感染的关系
- 批准号:
8084128 - 财政年份:2010
- 资助金额:
$ 115.8万 - 项目类别:
The Relationship of XMRV to Functional Status and Co-infections in Chronic Fatigu
XMRV 与慢性疲劳功能状态和合并感染的关系
- 批准号:
7977530 - 财政年份:2010
- 资助金额:
$ 115.8万 - 项目类别:
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