黄健男张瑞岩.基质金属蛋白酶在心肌缺血再灌注损伤中的作用[J].,2011,11(13):2584-2586 |
基质金属蛋白酶在心肌缺血再灌注损伤中的作用 |
Roleof Matrix Metalloproteinases in MyocardialIschemia-Reperfusion Injury |
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DOI: |
中文关键词: 基质金属蛋白酶 缺血再灌注 心肌损伤 |
英文关键词: Matrix metalloproteinases Ischemia-reperfusion Myocardial injury |
基金项目: |
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中文摘要: |
肌缺血再灌注损伤是指缺血心肌组织在恢复血流供给后,其细胞代谢功能障碍及结构破坏反而加重的现象,主要表现在心
肌收缩与舒张功能障碍、血管内皮功能障碍、微循环血流紊乱、细胞代谢失调、电解质平衡紊乱、细胞凋亡与坏死等,并伴随着氧
自由基的大量产生和毒性损伤以及炎症反应的激活,是一个极其复杂的病理过程。基质金属蛋白酶(MMPs) 及其组织抑制物
(TIMPs)是心肌组织中多种细胞分泌的内源性细胞因子,其作用涵盖了细胞外基质降解、炎症反应激活、调节血管功能、影响细胞
凋亡与存活等众多病理生理过程,而这些过程均在心肌缺血再灌注损伤中发挥着重要的作用。 |
英文摘要: |
Myocardial ischemia-reperfusion injury is syndrome that after blood supply restored in ischemic myocardium, cell
dysfunction and structural damage actually get worsen. It is very complicated and registers as myocardial systolic and diastolic
dysfunction, vascular endothelial dysfunction, microcirculation disorder, electrolyte balance disorder, cellular apoptosis and necrosis,
followed with generation of oxygen radicals and activation of inflammation. Matrix metalloproteinases and its tissue inhibitors are a
group of endogenous mediators expressed in heart tissues. They play an important role in many physiological processes, such as
extracellular matrix degradation, activation of inflammation, regulation of vascular function, cellular apoptosis and necrosis. All these
processes have a great relationship with myocardial ischemia-reperfusion injury. |
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