Kültz Dietmar
Physiological Genomics Group, Department of Animal Sciences, University of California, Davis, California 95616, USA.
Annu Rev Physiol. 2005;67:225-57. doi: 10.1146/annurev.physiol.67.040403.103635.
The cellular stress response is a universal mechanism of extraordinary physiological/pathophysiological significance. It represents a defense reaction of cells to damage that environmental forces inflict on macromolecules. Many aspects of the cellular stress response are not stressor specific because cells monitor stress based on macromolecular damage without regard to the type of stress that causes such damage. Cellular mechanisms activated by DNA damage and protein damage are interconnected and share common elements. Other cellular responses directed at re-establishing homeostasis are stressor specific and often activated in parallel to the cellular stress response. All organisms have stress proteins, and universally conserved stress proteins can be regarded as the minimal stress proteome. Functional analysis of the minimal stress proteome yields information about key aspects of the cellular stress response, including physiological mechanisms of sensing membrane lipid, protein, and DNA damage; redox sensing and regulation; cell cycle control; macromolecular stabilization/repair; and control of energy metabolism. In addition, cells can quantify stress and activate a death program (apoptosis) when tolerance limits are exceeded.
细胞应激反应是一种具有非凡生理/病理生理意义的普遍机制。它代表细胞对环境力量对大分子造成的损伤的防御反应。细胞应激反应的许多方面并非应激源特异性的,因为细胞基于大分子损伤来监测应激,而不考虑造成这种损伤的应激类型。由DNA损伤和蛋白质损伤激活的细胞机制相互关联并共享共同元件。针对重新建立内环境稳态的其他细胞反应是应激源特异性的,并且通常与细胞应激反应同时激活。所有生物体都有应激蛋白,普遍保守的应激蛋白可被视为最小应激蛋白质组。对最小应激蛋白质组的功能分析可产生有关细胞应激反应关键方面的信息,包括感知膜脂质、蛋白质和DNA损伤的生理机制;氧化还原传感与调节;细胞周期控制;大分子稳定/修复;以及能量代谢控制。此外,细胞可以量化应激,并在耐受极限被超过时激活死亡程序(凋亡)。