MMP-12 as an Endogenous Post-MI Resolution Promoting Factor
MMP-12 作为内源性 MI 后消退促进因子
基本信息
- 批准号:10327670
- 负责人:
- 金额:$ 38.13万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2019
- 资助国家:美国
- 起止时间:2019-02-01 至 2022-06-30
- 项目状态:已结题
- 来源:
- 关键词:AmericanAnti-Inflammatory AgentsApoptosisApoptoticBackCD44 geneCardiacCause of DeathCell physiologyCellsCicatrixCongestive Heart FailureCoupledDiagnosisDisciplineEnzymesEvaluationEventExcisionExtracellular MatrixFibroblastsFunctional disorderGasesGene ExpressionGoalsGrantHeartHeart failureHourHumanHyaluronic AcidImpairmentIn VitroIndividualInfarctionInflammationInflammatoryInfusion proceduresInterventionLeft Ventricular RemodelingLeft ventricular structureLeukocyte TraffickingLinkLipidsMME geneMediator of activation proteinModelingMolecularMusMyocardial InfarctionNecrosisOutcomeOxygenPatientsPhagocytosisPhenotypePhysiologyPlasmaProductionProteinsProteolysisProteomicsResolutionRoleSalineSignal PathwaySignal TransductionSmooth Muscle Actin Staining MethodSourceTestingTherapeuticTimeUnited Statescell typeimprovedin vivoinhibitorinnovationinterdisciplinary approachmacrophagemortalitynecrotic tissueneutrophilnoveloverexpressionpreventrepairedresponsetranscriptomicswound healing
项目摘要
Abstract
About one in four myocardial infarction (MI) patients progress to develop congestive heart failure, which
has a 5-year mortality rate of 50%. The goal of this project is to understand post-MI roles of matrix
metalloproteinase-12 (MMP-12) by establishing how MMP-12 serves as a resolution promoting factor to
stimulate the transition from inflammation to repair. We hypothesize that MMP-12 regulates individual
neutrophil, macrophage, and fibroblast physiology to promote the resolution of post-MI inflammation
and stimulate repair. Our specific aims will explore the mechanism whereby MMP-12 turns off pro-
inflammation (aim 1), initiates anti-inflammation (aim 2), and promotes repair (aim 3). Innovation lies in the
evaluation of MMP-12 post-MI to connect early cell functions to late remodeling outcomes and in the
integration of multi-discipline approaches to explore the mechanisms whereby MMP-12 regulates resolution.
This study will drive forward the understanding of the molecular basis of LV remodeling and will identify novel
intervention targets directed at MMP-12.
摘要
大约四分之一的心肌梗死(MI)患者进展为充血性心力衰竭,
五年死亡率为50%本项目的目标是了解矩阵的后MI角色
通过建立MMP-12如何作为促进因子,
刺激从炎症到修复的转变。我们假设MMP-12调节个体
中性粒细胞、巨噬细胞和成纤维细胞生理学促进MI后炎症消退
刺激修复我们的具体目标将探索MMP-12关闭亲的机制,
炎症(目的1),启动抗炎(目的2),并促进修复(目的3)。创新在于
评估MI后MMP-12将早期细胞功能与晚期重塑结果联系起来,
整合多学科方法,探索MMP-12调节消退的机制。
这项研究将推动对LV重构分子基础的理解,并将识别新的
针对MMP-12的干预目标。
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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MERRY L LINDSEY其他文献
MERRY L LINDSEY的其他文献
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{{ truncateString('MERRY L LINDSEY', 18)}}的其他基金
Short Course In Transferable Skills Training (SHIFT) Program
可转移技能培训短期课程 (SHIFT) 计划
- 批准号:
10725020 - 财政年份:2023
- 资助金额:
$ 38.13万 - 项目类别:
Systems Biology of Fibroblast Activation Following Myocardial Infarction
心肌梗塞后成纤维细胞激活的系统生物学
- 批准号:
9463789 - 财政年份:2016
- 资助金额:
$ 38.13万 - 项目类别:
Systems Biology of Fibroblast Activation Following Myocardial Infarction
心肌梗塞后成纤维细胞激活的系统生物学
- 批准号:
9119340 - 财政年份:2016
- 资助金额:
$ 38.13万 - 项目类别:
Systems Biology of Fibroblast Activation Following Myocardial Infarction
心肌梗塞后成纤维细胞激活的系统生物学
- 批准号:
9264010 - 财政年份:2016
- 资助金额:
$ 38.13万 - 项目类别:
A Community Effort to Translate Protein Data to Knowledge: An Integrated Platform
将蛋白质数据转化为知识的社区努力:一个集成平台
- 批准号:
9087292 - 财政年份:2014
- 资助金额:
$ 38.13万 - 项目类别:
A Community Effort to Translate Protein Data to Knowledge: An Integrated Platform
将蛋白质数据转化为知识的社区努力:一个集成平台
- 批准号:
8935858 - 财政年份:2014
- 资助金额:
$ 38.13万 - 项目类别:
A Community Effort to Translate Protein Data to Knowledge: An Integrated Platform
将蛋白质数据转化为知识的社区努力:一个集成平台
- 批准号:
8774362 - 财政年份:2014
- 资助金额:
$ 38.13万 - 项目类别:
A Community Effort to Translate Protein Data to Knowledge: An Integrated Platform
将蛋白质数据转化为知识的社区努力:一个集成平台
- 批准号:
9298691 - 财政年份:2014
- 资助金额:
$ 38.13万 - 项目类别:
MMP-9 Roles in the Aging Myocardial Response to Ischemia
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- 批准号:
8397507 - 财政年份:2009
- 资助金额:
$ 38.13万 - 项目类别:
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