Cardiovascular Immunology Research Core (Core B)
心血管免疫学研究核心(核心B)
基本信息
- 批准号:10625951
- 负责人:
- 金额:$ 24.6万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2023
- 资助国家:美国
- 起止时间:2023-04-05 至 2028-03-31
- 项目状态:未结题
- 来源:
- 关键词:Adaptor Signaling ProteinAdultAntibodiesAntigen-Antibody ComplexBindingBiological ProcessCardiacCardiac MyocytesCardiovascular systemCell AgingCell Cycle ArrestCellsCessation of lifeChromiumComplexConsultationsCyclic GMPDNAData AnalysesDigestionEnzymesEquipmentFailureFlow CytometryGene Expression ProfilingGenerationsGenomicsGoalsGrowthHeartHeart failureHyperplasiaHypertrophyImmuneImmune responseImmunologicsImmunologistImmunologyImmunology procedureInflammatory ResponseInjuryInnate Immune ResponseInterferon Type IInterferonsIsomerismLifeLinkLogisticsMacrophageMediatingMedical centerModelingMyocardialNatural ImmunityNatural regenerationNeonatalPathway interactionsPlayProcessProductionProductivityProliferatingReagentRegulationRejuvenationResearchResearch DesignResearch PersonnelResource AllocationResourcesRoleSecond Messenger SystemsServicesSignal TransductionStimulator of Interferon GenesT-LymphocyteTechnical ExpertiseTechniquesTherapeuticTissuesTumor ImmunityVentricular RemodelingVirusWestern Blottingdesignexperiencegain of functionhealingimmunocytochemistryinhibitorinnovationinterestloss of functionmeetingsmemberpostnatalpreventprogramsresponse to injurysensorsingle-cell RNA sequencingskillssuccesssynergism
项目摘要
Heart failure progression is a complex biological process that is precipitated by the maladaptive myocardial
response to injury, compounded by failure of the adult heart to replace lost or damaged cardiomyocytes.
Conceivably, identifying common pathways that regulate these two seemingly unrelated processes would
profoundly impact therapeutic strategies to prevent, and even reverse heart failure progression. Numerous
observations by members of the proposed consortium and others support the notion that the endogenous
capacity of the neonatal mammalian heart to proliferate fades in the early postnatal life as a switch from
hyperplastic to hypertrophic growth of cardiomyocytes takes place. Members of the proposed consortium and
others have also previously demonstrated that mechanisms linked to activation of innate immune response may
play a role in cardiomyocyte hypertrophy, death and even stimulation of new cardiomyocyte
generation. However, whether mechanisms involved in cardiomyocyte cell cycle arrest also play a role in the
maladaptive cardiomyocyte response to injury is not known. Indeed, critical components of the inflammatory
response appear to underlie both cardiac rejuvenation after injury through positive effects on healing, as well
as stimulating cardiomyocytes to proliferate. Therefore, the current proposal brings together 5 groups with
expertise in myocardial remodeling, regeneration and immunology with the overall goal of determining the role
of immune response signaling in regulation of cardiac growth and regeneration. The 4 Project Leaders are
cardiovascular biologist, and thus having a strong immunology presence in the network is paramount for its
success, not only to provide technical expertise and reagents, but also to play a crucial consultancy role. Core
B will be led by Dr. James Chen, a renowned immunologist, who will play the critical role of providing technical
and logistic support to Project Leaders in all matters pertaining to immunological studies. This is a critical and
innovative design of the current Program Project as it will allow the 4 Project leaders to seamlessly integrate
complex immunological assays and concepts into their research program. As such, Core B will provide a
number of essential support services including isolation and characterization of immune cells, performing gene
expression analysis studies, providing critical reagents for immunological assays and providing consultation on
study design and interpretation. The immunology goal will serve an invaluable role within the network that will
enhance synergy, and maximize productivity of all Network Projects
心力衰竭进展是一个复杂的生物学过程,由不良适应性心肌沉淀
对损伤的反应,由于成人心脏无法替代损失或受损的心肌细胞的损失而复杂化。
可以想象,确定调节这两个看似无关的过程的通用途径将
深刻影响治疗策略,以预防甚至逆转心力衰竭进展。很多的
拟议财团和其他人的观察结果支持内源性的观念
新生儿哺乳动物心脏的能力在产后早期的生命中逐渐消失,因为
发生心肌细胞的增生至肥厚性生长。拟议财团的成员和
其他人先前还证明了与先天免疫反应激活有关的机制可能
在心肌细胞肥大,死亡甚至刺激新心肌细胞中发挥作用
一代。但是,涉及心肌细胞细胞周期停滞的机制是否也在
适应不良的心肌细胞对损伤的反应尚不清楚。确实,炎症的关键成分
反应似乎是通过对愈合的积极影响受伤后两种心脏复兴的基础
作为刺激心肌细胞增殖。因此,当前的提议将5组汇集在一起
心肌重塑,再生和免疫学的专业知识,其总体目标是确定角色
在调节心脏生长和再生中的免疫反应信号传导。 4个项目负责人是
心血管生物学家,因此在网络中具有强大的免疫学存在至关重要
成功,不仅提供技术专长和试剂,而且还发挥着关键的咨询作用。核
B将由著名免疫学家詹姆斯·陈(James Chen)主持,他将发挥提供技术的关键作用
在与免疫学研究有关的所有事项中,对项目领导者的逻辑支持。这是一个关键,
当前计划项目的创新设计,因为这将使4位项目负责人无缝整合
复杂的免疫学测定和概念的研究计划。因此,核心B将提供
基本支持服务的数量,包括免疫细胞的隔离和表征,执行基因
表达分析研究,为免疫学分析提供关键试剂,并就
研究设计和解释。免疫学目标将在网络中发挥无价的作用
增强协同作用并最大化所有网络项目的生产力
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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Zhijian J Chen其他文献
Zhijian J Chen的其他文献
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{{ truncateString('Zhijian J Chen', 18)}}的其他基金
Biochemical Dissection of the RIG-I Antiviral Pathway
RIG-I 抗病毒途径的生化剖析
- 批准号:
8602822 - 财政年份:2011
- 资助金额:
$ 24.6万 - 项目类别:
Biochemical Dissection of the RIG-I Antiviral Pathway
RIG-I 抗病毒途径的生化剖析
- 批准号:
8225150 - 财政年份:2011
- 资助金额:
$ 24.6万 - 项目类别:
Biochemical Dissection of the RIG-I Antiviral Pathway
RIG-I 抗病毒途径的生化剖析
- 批准号:
8810636 - 财政年份:2011
- 资助金额:
$ 24.6万 - 项目类别:
Biochemical Dissection of the RIG-I Antiviral Pathway
RIG-I 抗病毒途径的生化剖析
- 批准号:
8416440 - 财政年份:2011
- 资助金额:
$ 24.6万 - 项目类别:
Biochemical Dissection of the RIG-I Antiviral Pathway
RIG-I 抗病毒途径的生化剖析
- 批准号:
8087900 - 财政年份:2011
- 资助金额:
$ 24.6万 - 项目类别:
Mechanisms of NF-kappaB Activation in T Lymphocytes
T 淋巴细胞中 NF-κB 激活的机制
- 批准号:
7435307 - 财政年份:2004
- 资助金额:
$ 24.6万 - 项目类别:
Mechanisms of NF-kappaB Activation in T Lymphocytes
T 淋巴细胞中 NF-κB 激活的机制
- 批准号:
6898227 - 财政年份:2004
- 资助金额:
$ 24.6万 - 项目类别:
Mechanisms of NF-kappaB Activation in T Lymphocytes
T 淋巴细胞中 NF-κB 激活的机制
- 批准号:
7069593 - 财政年份:2004
- 资助金额:
$ 24.6万 - 项目类别:
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