Kucharzewski Marek, Sieroń Aleksander, Kowalczyk Jacek
Pol Merkur Lekarski. 2003 Sep;15(87):213-6.
Heat-shock proteins (HSP) are a group of highly conserved proteins, which production is induced as a intracellular response to different kinds of stresses. They are also included in the group of chaperones, which are involved in protein folding and refolding in the cells, stabilising of macromolecular structure and repairing of denatured proteins or promoting their degradation when damages are too advanced. Because of protective role of HSP on the cellular level, a lot of studies is focused on the place of HSP in cardioprotection. The exact mechanism of this activity is still unknown. The experiments provided convincing proofs that cardiomyocytes which were subjected to hyperthermia or many other stress factors were reacting increased synthesis of HSP what guaranteed protection against further, stronger episodes of different stresses. The problem, which is still actual, is finding the possibility of taking advantage of cardioprotective properties of HSP in the treatment. Such a situation is due to lack of noninvasive methods of inducing HSP expression. The present study is a kind of review of literature taking up this problem, starting with protocols using hyperthermia, through the pharmacological therapy and ending with molecular techniques and genetic engineering.
热休克蛋白(HSP)是一组高度保守的蛋白质,其产生是作为细胞对各种应激的一种胞内反应而被诱导的。它们也属于伴侣蛋白组,参与细胞内蛋白质的折叠和重折叠、大分子结构的稳定以及变性蛋白质的修复,或者在损伤过于严重时促进其降解。由于热休克蛋白在细胞水平上的保护作用,许多研究聚焦于热休克蛋白在心脏保护中的作用。这种活性的确切机制仍然未知。实验提供了令人信服的证据,即经历过热或许多其他应激因素的心肌细胞会通过增加热休克蛋白的合成做出反应,从而保证对进一步更强的不同应激发作具有保护作用。目前仍然实际存在的问题是,在治疗中找到利用热休克蛋白心脏保护特性的可能性。这种情况是由于缺乏诱导热休克蛋白表达的非侵入性方法。本研究是对涉及该问题的文献的一种综述,从使用热疗的方案开始,经过药物治疗,最后以分子技术和基因工程结束。