Trautinger F
University of Vienna, Division of Special and Environmental Dermatology, Department of Dermatology, Währinger Gürtel 18-20, A-1090 Vienna, Austria.
J Photochem Photobiol B. 2001 Oct;63(1-3):70-7. doi: 10.1016/s1011-1344(01)00203-2.
All organisms respond to sudden environmental changes with the increased transcription of genes belonging to the family of heat shock proteins (hsps). Hsp-inducing stress factors include elevated temperatures, alcohol, heavy metals, oxidants, and agents leading to protein denaturation. The induction of heat shock proteins is followed by a transient state of increased resistance to further stress and the heat shock response is generally thought to represent an evolutionary conserved adaptive mechanism to cope with hostile environmental conditions. Since the skin as a barrier organ has to cope with the potentially harmful consequences of exposure to ultraviolet radiation (UV), it appears reasonable to question whether hsps constitute a natural defence mechanism against UV. Hsps have been detected in resting as well as in stressed epidermal and dermal cells and overexpression of hsps is associated with increased resistance to UV-induced cell death. Furthermore, UV itself is able to induce the expression of specific hsps. Thus, hsps might provide an adaptive cellular response to increasing UV and enhancing the expression of hsps might turn out as a new way to deal with the immediate and long-term consequences of UV exposure. Prerequisite for the utilization of this concept is the development of non-toxic heat shock inducers and their evaluation for clinical efficacy and safety.
所有生物体都会通过增加热休克蛋白（hsps）家族基因的转录来应对突然的环境变化。诱导hsps的应激因素包括温度升高、酒精、重金属、氧化剂以及导致蛋白质变性的物质。热休克蛋白的诱导之后会出现对进一步应激的抵抗力增强的短暂状态，并且热休克反应通常被认为是一种进化上保守的适应机制，以应对恶劣的环境条件。由于皮肤作为一个屏障器官必须应对暴露于紫外线（UV）的潜在有害后果，因此质疑hsps是否构成针对UV的天然防御机制似乎是合理的。在静止以及应激的表皮和真皮细胞中都检测到了hsps，并且hsps的过表达与对UV诱导的细胞死亡的抵抗力增加有关。此外，UV本身能够诱导特定hsps的表达。因此，hsps可能为增加的UV提供一种适应性细胞反应，并且增强hsps的表达可能成为应对UV暴露的即时和长期后果的一种新方法。利用这一概念的前提是开发无毒的热休克诱导剂并对其临床疗效和安全性进行评估。
