Cardiovascular Peptides and Myocardial Infarction

心血管肽与心肌梗塞

基本信息

  • 批准号:
    7269302
  • 负责人:
  • 金额:
    $ 49.17万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2006
  • 资助国家:
    美国
  • 起止时间:
    2006-08-01 至 2010-07-31
  • 项目状态:
    已结题

项目摘要

DESCRIPTION (provided by applicant): Our objective is to establish that the cardiac peptide BNP is a novel and efficacious therapy for human acute myocardial infarction (AMI) to preserve myocardial structure and function. This highly translational research takes advantage of the cardioprotective and renal enhancing properties of this small and endogenous peptide in protecting the heart from injury and promoting cardiac repair. Our broad unifying hypothesis is that the endogenous natriuretic peptide (NP) system mediates cardiorenal protection and that therapeutic enhancement in experimental and human AMI with exogenous BNP will preserve myocardial structure and function while maintaining renal function. This strategy is based on the biology of BNP that enhances renal function, mediates coronary vasodilatation, reduces myocardial oxygen consumption, suppresses aldosterone release, retards adrenergic activation, induces vascular regeneration, inhibits cardiac fibroblast collagen synthesis and has anti-apoptotic properties. First, we will utilize a murine model of partial proANP gene disruption (Nppa+/-) that has clinical relevance to the recently reported human polymorphism (C664G) that is reported to be characterized by a distruption of the ANP promoter with reduced circulating ANP and risk for ventricular remodeling in human hypertension. This novel genetically altered model has normal cardiac phenotype but demonstrates an exaggerated ventricular hypertrophic and fibrotic response to AMI. In this model with AMI and in wild type (WT) mice we seek to establish cardiorenal protection with 5 days of BNP based therapy. Second, we will extend our research to human AMI investigating the cardiorenal protective properties of 72 hours of BNP therapy initiated at the time of revascularization compared to conventional therapy to preserve myocardial and renal function. Our Specific Aims are as follows: Aim 1: To characterize myocardial structure and function, humoral function and renal function in WT and Nppa+/- mice after AMI; Aim 2: To characterize myocardial structure and function, humoral function and renal function in WT and Nppa+/- mice after AMI in the presence of BNP therapy; and Aim 3: To characterize myocardial structure and function, humoral function and renal function in human AMI in the presence and absence of BNP therapy. For the public, this research may enhance long-term survival after a heart attack. The use of a hormone made in the heart and given at the time of heart attack may help the heart protect and repair itself.
DESCRIPTION (provided by applicant): Our objective is to establish that the cardiac peptide BNP is a novel and efficacious therapy for human acute myocardial infarction (AMI) to preserve myocardial structure and function. This highly translational research takes advantage of the cardioprotective and renal enhancing properties of this small and endogenous peptide in protecting the heart from injury and promoting cardiac repair. Our broad unifying hypothesis is that the endogenous natriuretic peptide (NP) system mediates cardiorenal protection and that therapeutic enhancement in experimental and human AMI with exogenous BNP will preserve myocardial structure and function while maintaining renal function. This strategy is based on the biology of BNP that enhances renal function, mediates coronary vasodilatation, reduces myocardial oxygen consumption, suppresses aldosterone release, retards adrenergic activation, induces vascular regeneration, inhibits cardiac fibroblast collagen synthesis and has anti-apoptotic properties. First, we will utilize a murine model of partial proANP gene disruption (Nppa+/-) that has clinical relevance to the recently reported human polymorphism (C664G) that is reported to be characterized by a distruption of the ANP promoter with reduced circulating ANP and risk for ventricular remodeling in human hypertension. This novel genetically altered model has normal cardiac phenotype but demonstrates an exaggerated ventricular hypertrophic and fibrotic response to AMI. In this model with AMI and in wild type (WT) mice we seek to establish cardiorenal protection with 5 days of BNP based therapy. Second, we will extend our research to human AMI investigating the cardiorenal protective properties of 72 hours of BNP therapy initiated at the time of revascularization compared to conventional therapy to preserve myocardial and renal function. Our Specific Aims are as follows: Aim 1: To characterize myocardial structure and function, humoral function and renal function in WT and Nppa+/- mice after AMI; Aim 2: To characterize myocardial structure and function, humoral function and renal function in WT and Nppa+/- mice after AMI in the presence of BNP therapy; and Aim 3: To characterize myocardial structure and function, humoral function and renal function in human AMI in the presence and absence of BNP therapy. For the public, this research may enhance long-term survival after a heart attack. The use of a hormone made in the heart and given at the time of heart attack may help the heart protect and repair itself.

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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John C Burnett其他文献

cGMP enhancing strategies for acute and chronic heart failure
  • DOI:
    10.1186/1471-2210-5-s1-s22
  • 发表时间:
    2005-06-16
  • 期刊:
  • 影响因子:
    2.700
  • 作者:
    John C Burnett;Guido Boerrigter
  • 通讯作者:
    Guido Boerrigter
Integrin receptor subtype antagonism augments BNP-mediated cGMP generation in cultured human cardiac fibroblasts: evidence for particulate guanylate cyclase receptor and integrin receptor cross-talk
  • DOI:
    10.1186/1471-2210-7-s1-p30
  • 发表时间:
    2007-07-25
  • 期刊:
  • 影响因子:
    2.700
  • 作者:
    Brenda K Huntley;John C Burnett
  • 通讯作者:
    John C Burnett
Pharmacokinetic and pharmacodynamic study of a novel chimeric natriuretic peptide, CD-NP, in the normal dog
  • DOI:
    10.1186/1471-2210-7-s1-p38
  • 发表时间:
    2007-07-25
  • 期刊:
  • 影响因子:
    2.700
  • 作者:
    Candace YW Lee;Guido Boerrigter;Gail J Harty;John C Burnett
  • 通讯作者:
    John C Burnett
Bioavailability of intravenous versus subcutaneous administration of the dual GC-A and GC-B designer natriuretic peptide cenderitide in healthy canines
  • DOI:
    10.1186/1471-2210-11-s1-p11
  • 发表时间:
    2011-08-01
  • 期刊:
  • 影响因子:
    2.700
  • 作者:
    Guido Boerrigter;Lisa C Costello-Boerrigter;Gail J Harty;John C Burnett
  • 通讯作者:
    John C Burnett

John C Burnett的其他文献

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{{ truncateString('John C Burnett', 18)}}的其他基金

Novel Therapeutics for Cardiovascular Disease
心血管疾病的新疗法
  • 批准号:
    10440006
  • 财政年份:
    2022
  • 资助金额:
    $ 49.17万
  • 项目类别:
Novel Peptide Therapeutics for Hypertension
高血压的新型肽疗法
  • 批准号:
    10077576
  • 财政年份:
    2018
  • 资助金额:
    $ 49.17万
  • 项目类别:
Novel Peptide Therapeutics for Cardiorenal Protection in Heart Failure
用于心力衰竭心肾保护的新型肽疗法
  • 批准号:
    9753353
  • 财政年份:
    2017
  • 资助金额:
    $ 49.17万
  • 项目类别:
Novel Peptide Therapeutics for Cardiorenal Protection in Heart Failure
用于心力衰竭心肾保护的新型肽疗法
  • 批准号:
    9211673
  • 财政年份:
    2017
  • 资助金额:
    $ 49.17万
  • 项目类别:
Small Molecule Discovery for GC-A Activators
GC-A 激活剂的小分子发现
  • 批准号:
    8962993
  • 财政年份:
    2015
  • 资助金额:
    $ 49.17万
  • 项目类别:
Protein Therapeutics to Prevent Heart Failure Post Myocardial Infarction
预防心肌梗塞后心力衰竭的蛋白质疗法
  • 批准号:
    8020951
  • 财政年份:
    2010
  • 资助金额:
    $ 49.17万
  • 项目类别:
Protein Therapeutics to Prevent Heart Failure Post Myocardial Infarction
预防心肌梗塞后心力衰竭的蛋白质疗法
  • 批准号:
    7867072
  • 财政年份:
    2010
  • 资助金额:
    $ 49.17万
  • 项目类别:
Natriuretic Peptide System and Cardiac Fibrosis
利钠肽系统与心脏纤维化
  • 批准号:
    7898654
  • 财政年份:
    2009
  • 资助金额:
    $ 49.17万
  • 项目类别:
Core--Neurohumoral
核心--神经体液
  • 批准号:
    7898658
  • 财政年份:
    2009
  • 资助金额:
    $ 49.17万
  • 项目类别:
Cardiovascular Peptides and Myocardial Infarction
心血管肽与心肌梗塞
  • 批准号:
    7476465
  • 财政年份:
    2006
  • 资助金额:
    $ 49.17万
  • 项目类别:

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肾上腺素能药物治疗AD疗效的临床前试验
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