热休克蛋白(HSP)作为分子伴侣的防御机制首先需要热休克转录因子作为热休克反应的媒介。HSP的过度表达有心肌保护作用,能阻碍心肌细胞凋亡、保护缺血时心肌细胞微管和肌动蛋白骨架以及内皮细胞的完整性、参与蛋白激酶和转录因子如缺氧诱导转录因子(HIF)-1α和热休克转录因子(HSF1)的折叠和激活、黏附NO合成酶以及刺激其活性,还可能下调细胞因子产物。因此,避免任何不良反应,并采用药理学和基因治疗的程序诱导心肌中HSP水平的升高在心肌保护中有重要意义。 Heat shock protein (HSP) as a chaperone defense mechanism first needs heat shock transcription factor as a heat shock response mediator. Overexpression of HSP has cardioprotective effects that can block cardiomyocyte apoptosis, protect the integrity of myocyte microtubules and actin cytoskeleton and endothelial cells during ischemia, and is involved in the regulation of protein kinases and transcription factors such as hypoxia-inducible transcription factor (HIF) ) -1α and heat shock transcription factor (HSF1), adhesion and stimulation of NO synthase, may also down-regulate cytokine production. Therefore, avoiding any adverse reactions and using pharmacological and gene therapy programs to induce elevated levels of HSP in myocardium is of great importance in myocardial protection.