课题基金 / 基金详情

STRESS PROTEIN 60 DURING MYOCARDIAL ISCHEMIA

STRESS PROTEIN 60 DURING MYOCARDIAL ISCHEMIA
心肌缺血期间的应激蛋白 60
批准号:
2211222
负责人:
RUBEN MESTRIL
金额:
$10.66万
依托单位国家:
美国
项目类别:
财政年份:
1994
资助国家:
美国
项目状态:
已结题
起止时间:
1994-08-01 至 1998-07-31

项目摘要

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中文摘要
翻译
冠状动脉疾病可导致慢性心力衰竭,需要
英文摘要
Coronary artery disease can lead to chronic heart failure, need for revascularization (by-pass surgery), or life-threatening cardiac arrhythmias. It is the cause of one and a half million acute myocardial infarctions per year in the USA, more than half of them lethal. Its cost is the highest of all Current medical diseases in the nation. Coronary artery disease affects the blood supply of the heart muscle (myocardium) and, therefore, decreases oxygen delivery to myocardial cells. The mitochondria of cardiac myocytes is one of the major targets for ischemia- induced damage. Limitations of oxygen delivery reduces mitochondrial oxidative phosphorylation and contributes to the reduction of intracellular ATP levels. Some investigators have indicated that the inability of the mitochondria to self-repair following restoration of blood flow may be one of the crucial events leading to the ultimate death of myocardial cells. Although it is not clear if sarcolemmal or mitochondrial damage is the main event in the irreversible damage of the myocardial cell, the role of mitochondrial changes in decreased myocardial functions are not questioned. Recent studies have shown that heat shock protein (HSP) 60, which is a member of the stress protein family and are thought to have a protective role during oxidative stress, is required for the assembly of multimeric enzyme complexes within the mitochondria. We have recently found that during acute occlusion of the descending coronary artery for 30 minutes in the rat heart, which leads to ischemia in the left ventricle, there is a marked and specific increase in HSP6O mRNA level. This finding leads us to believe that HSP6O as other related HSPs may have a protective role and is probably involved in the repair of the mitochondrial enzymatic complexes vital for the normal function of the mitochondria. It is our objective to investigate this ischemia-induced change in HSP6O expression and determine if HSP60 mediates protection processes in the mitochondria that contribute to recovery from ischemic injury in the myocardial cell.
期刊论文(7)
专著(0)
科研奖励(0)
会议论文
Endothelium-derived relaxing factor contributes to the regulation of endothelial permeability.
内皮源性舒张因子有助于内皮通透性的调节。
DOI: 10.1002/jcp.1041510309
发表时间: 1992
期刊: Journal of cellular physiology
影响因子: 5.6
作者: [Oliver,JA]
通讯作者: Oliver,JA
Synthesis of angiotensinogen by renin-containing neuroblastomas.
含肾素的神经母细胞瘤合成血管紧张素原。
DOI: 10.1152/ajpcell.1989.257.2.c185
发表时间: 1989
期刊: The American journal of physiology
影响因子: --
作者: [Petrossian,G, Oliver,JA]
通讯作者: Oliver,JA
Changes in luminal flow rate modulate basal and bradykinin-stimulated cell [Ca2+] in aortic endothelium.
管腔流速的变化调节主动脉内皮细胞的基础细胞和缓激肽刺激细胞 [Ca2+]。
DOI: 10.1002/jcp.1041510107
发表时间: 1992
期刊: Journal of cellular physiology
影响因子: 5.6
作者: [Oliver,JA, ChaseJr,HS]
通讯作者: ChaseJr,HS
Stable expression of a human HSP70 gene in a rat myogenic cell line confers protection against endotoxin.
人类 HSP70 基因在大鼠生肌细胞系中的稳定表达可提供针对内毒素的保护。
DOI: 10.1152/ajpcell.1996.270.4.c1017
发表时间: 1996
期刊: The American journal of physiology.
影响因子: --
作者: [Chi,SH, Mestril,R]
通讯作者: Mestril,R
Cardioprotection against endotoxins
  • 批准号:
    6769959
  • 项目类别:
  • 资助金额:
    $25.9万
  • 财政年份:
    2003
  • 负责人:
    RUBEN MESTRIL
  • 依托单位:
Cardioprotection against endotoxins
  • 批准号:
    6895802
  • 项目类别:
  • 资助金额:
    $25.9万
  • 财政年份:
    2003
  • 负责人:
    RUBEN MESTRIL
  • 依托单位:
Cardioprotection against endotoxins
  • 批准号:
    6669618
  • 项目类别:
  • 资助金额:
    $28.4万
  • 财政年份:
    2003
  • 负责人:
    RUBEN MESTRIL
  • 依托单位:
Cardioprotection against endotoxins
  • 批准号:
    7069035
  • 项目类别:
  • 资助金额:
    $25.29万
  • 财政年份:
    2003
  • 负责人:
    RUBEN MESTRIL
  • 依托单位:
海外基金