Heart Failure: Genetics, Genomics and Epigenetics
Heart Failure: Genetics, Genomics and Epigenetics
批准号:
9049783
负责人:
DAVID L. WOODLAND
金额:
$1.2万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
2016
资助国家:
美国
项目状态:
已结题
起止时间:
2016-03-01 至 2016-11-15
关键词:
AddressArchitectureBioinformaticsBiological MarkersBiological ModelsBiologyBiotechnologyCardiac developmentCellsClinicalCollaborationsCommunitiesData SetDiagnosisDiastolic heart failureDiseaseDisease ProgressionDisease modelEpidemicEpigenetic ProcessEtiologyGenesGeneticGenomicsHeart failureHumanIndustryInvestmentsJointsKnowledgeMethodologyMicroRNAsMolecularMuscle CellsNatural regenerationOutcomeParticipantPathogenesisPharmacologic SubstancePredispositionResearchResearch PersonnelRoleScientistSignal PathwayTherapeuticTimeTraining ProgramsTranslationsTreatment CostUtahWorkbasecatalystclinical practicecookinghuman diseaseinduced pluripotent stem cellinnovationinsightmeetingsnovel strategiesposterspreventprogramsrepairedstem cell therapysymposium
中文摘要
描述(由申请人提供):申请支持由Stuart A.Cook、Christine E.Seidman和Yigal M.Pinto组织的题为心力衰竭:遗传学、基因组学和表观遗传学的Keystone研讨会。会议将于2016年4月3日至7日在犹他州雪鸟举行。心力衰竭(HF)是一种世界性流行病,每年的治疗费用高达数百亿美元。尽管有这样的投资,HF疗法在减少疾病进展方面的效果有限。在基础心肌细胞生物学、心力衰竭病因和发病机制方面的最新见解正在推动治疗和预防心力衰竭的新策略。这次会议将探讨生物和技术的进展,揭示遗传结构、分子发病机制和治疗心力衰竭的创新方法。这是在非常大的人类高频数据集可用,并可以使用先进的计算和生物信息学方法进行询问的时候出现的。具体目标是:1)考虑与人类收缩和舒张期心力衰竭有关的基因、分子、信号通路和生物标志物;2)在模型系统中探索心力衰竭的发病机制;3)了解表观遗传学、miRNAs和lncRNAs在心力衰竭发病机制中的作用;以及4)综述基因组学、药理学和基于细胞的疗法中治疗心力衰竭的翻译程序。这次会议的结果应该对基础、翻译和临床社区产生深远的影响。会议还应该为初级科学家提供一个很好的培训计划,并成为研究、临床和工业参与者之间合作的催化剂。这次会议与心脏发育、再生和修复会议同时举行,该会议为遗传学、IPSC疾病建模、干细胞疗法和表观遗传学的联合会议提供了一个绝佳的机会。
英文摘要
DESCRIPTION (provided by applicant): Support is requested for a Keystone Symposia meeting entitled Heart Failure: Genetics, Genomics and Epigenetics, organized by Stuart A. Cook, Christine E. Seidman and Yigal M. Pinto. The meeting will be held in Snowbird, Utah from April 3-7, 2016. Heart failure (HF) is a worldwide epidemic with treatments costing tens of billions of dollars every year. Despite this investment, HF therapies have limited efficacy in reducing disease progression. Recent insights in fundamental myocyte biology, HF etiologies and pathogenic mechanisms are propelling new strategies to treat and prevent HF. This meeting will explore biologic and technical advances that inform the genetic architecture, molecular pathogenesis and innovative approaches to treat HF. This comes at a time when very large human HF datasets are available and can be interrogated using advanced computational and bioinformatic approaches. Specific aims are to: 1) Consider genes, molecules, signaling pathways and biomarkers involved in systolic and diastolic HF in humans; 2) Explore disease mechanisms underlying HF in model systems; 3) Understand the role of epigenetics, miRNAs and lncRNAs in HF pathogenesis; and 4) Review translational programs in genomic, pharmacologic and cell-based therapeutics to treat HF. The outcomes of this meeting should be far-reaching for basic, translational and clinical communities. The meeting should also provide an excellent training program for junior scientists and serve as a catalyst for collaboration among research, clinical and industrial participants. This meeting is being held in conjunction with the Cardiac Development, Regeneration and Repair meeting that provides an outstanding opportunity for joint sessions in genetics, iPSC disease modeling, stem cell therapeutics and epigenetics.
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