Role of JNK and BNP in Septic Hypotension

JNK 和 BNP 在脓毒性低血压中的作用

基本信息

  • 批准号:
    10265517
  • 负责人:
  • 金额:
    $ 36.58万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2020
  • 资助国家:
    美国
  • 起止时间:
    2020-09-20 至 2023-08-31
  • 项目状态:
    已结题

项目摘要

Modified Project Summary/Abstract Section Sepsis is the body’s overwhelming immune response to infection that leads to organ failure and death. Refractory hypotension despite administration of vasopressors and fluid resuscitation is the most severe consequence of sepsis with a ~50% in-hospital mortality rate. Currently, there are no targeted therapies to treat sepsis. Existing treatment guidelines focus on source control and supportive care, including early administration of antibiotics and fluid resuscitation. Thus, novel genes and pathways that are involved in the pathophysiology of sepsis are actively sought with the goal to identify new targets that may offer novel therapeutic approaches. Cardiac dysfunction and hypotension in sepsis are associated with poor prognosis and increased mortality. Elevated circulating levels of B-type natriuretic peptide (BNP) correlate with myocardial stress in sepsis, as well as in other types of heart failure. Our data identified a signaling pathway that increased BNP production leads to lower cardiac output. Our previous studies and new data show that cardiac JNK activation, which we have shown to be involved in sepsis pathophysiology, increases BNP expression in septic mice. Our new data show that JNK inhibition increases blood pressure and tissue perfusion in septic mice and this is associated with lower plasma BNP levels. Thus, our central hypothesis is that inhibition of circulating BNP will alleviate septic hypotension and improve survival. To address our hypothesis we have designed the following specific aim: Aim 1 - To assess the role of BNP in reducing CO and promoting hypotension in septic mice and patients. In summary, our goal is to elucidate the role of BNP in the pathophysiology of septic hypotension and explore the therapeutic potential of treatment strategies aimed at regulating BNP expression or neutralizing circulating BNP. Simultaneously, we will pursue clinical studies to evaluate the translational impact of our findings. Thus, we anticipate our findings to constitute the basis for designing future clinical applications aiming to alleviate septic hypotension and organ hypo-perfusion.
修改的项目摘要/摘要部分

项目成果

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Konstantinos Drosatos其他文献

Konstantinos Drosatos的其他文献

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{{ truncateString('Konstantinos Drosatos', 18)}}的其他基金

Role of cardiomyocyte KLF5 in heart failure
心肌细胞KLF5在心力衰竭中的作用
  • 批准号:
    10666690
  • 财政年份:
    2022
  • 资助金额:
    $ 36.58万
  • 项目类别:
Role of cardiomyocyte KLF5 in heart failure
心肌细胞KLF5在心力衰竭中的作用
  • 批准号:
    10591922
  • 财政年份:
    2022
  • 资助金额:
    $ 36.58万
  • 项目类别:
Role of JNK and BNP in Septic Hypotension
JNK 和 BNP 在脓毒性低血压中的作用
  • 批准号:
    10389857
  • 财政年份:
    2020
  • 资助金额:
    $ 36.58万
  • 项目类别:
Role of KLF5 in cardiac and systemic fatty acid metabolism
KLF5 在心脏和全身脂肪酸代谢中的作用
  • 批准号:
    9919371
  • 财政年份:
    2016
  • 资助金额:
    $ 36.58万
  • 项目类别:
Role of KLF5 in cardiac and systemic fatty acid metabolism
KLF5 在心脏和全身脂肪酸代谢中的作用
  • 批准号:
    9006831
  • 财政年份:
    2016
  • 资助金额:
    $ 36.58万
  • 项目类别:
Mechanisms of Reduced Fatty Acid Oxidation and Cardiac Dysfunction in Sepsis
脓毒症中脂肪酸氧化减少和心脏功能障碍的机制
  • 批准号:
    8470701
  • 财政年份:
    2012
  • 资助金额:
    $ 36.58万
  • 项目类别:
Mechanisms of Reduced Fatty Acid Oxidation and Cardiac Dysfunction in Sepsis
脓毒症中脂肪酸氧化减少和心脏功能障碍的机制
  • 批准号:
    8828402
  • 财政年份:
    2012
  • 资助金额:
    $ 36.58万
  • 项目类别:
Mechanisms of Reduced Fatty Acid Oxidation and Cardiac Dysfunction in Sepsis
脓毒症中脂肪酸氧化减少和心脏功能障碍的机制
  • 批准号:
    9088504
  • 财政年份:
    2012
  • 资助金额:
    $ 36.58万
  • 项目类别:
Mechanisms of Reduced Fatty Acid Oxidation and Cardiac Dysfunction in Sepsis
脓毒症中脂肪酸氧化减少和心脏功能障碍的机制
  • 批准号:
    8278334
  • 财政年份:
    2012
  • 资助金额:
    $ 36.58万
  • 项目类别:

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