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紫外线照射后热休克蛋白在皮肤中的意义。

Significance of heat shock proteins in the skin upon UV exposure.

作者信息

Jonak Constanze, Klosner Gabriele, Trautinger Franz

机构信息

Department of Dermatology, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria.

出版信息

Front Biosci (Landmark Ed). 2009 Jan 1;14(12):4758-68. doi: 10.2741/3565.

Abstract

The expression of heat shock proteins (Hsp) expression is induced in all cells by exposure to heat and other environmental stress and Hsp can protect cells from damage through further exposure. Hsp are highly conserved and it is likely that they are essential for survival in a potentially harmful environment. Most Hsp are molecular chaperones sensing unfolded proteins and mediating their re-folding, transport, and interaction. In human epidermis Hsp are associated with differentiation, photoprotection, and skin disease. Recent research has mainly focused on the 27kD and 72kD Hsp that are constitutively expressed in keratinocytes. Cell death induced by ultraviolet radiation (UV) can be inhibited by previous heat shock and UV itself can induce Hsp experimentally. Regulation of Hsp can be pharmacologically modified and topical and systemic inducers and inhibitors of Hsp expression are under development. Whether phototherapy exerts its clinical efficacy by modulation of Hsp has not been sufficiently studied. The UV-wavelength ranges, -intensities and -doses that are required to interfere with the heat shock response in the skin still remain to be elucidated.

摘要

热休克蛋白(Hsp)的表达可在所有细胞中由热暴露和其他环境应激诱导产生,并且Hsp可通过进一步暴露保护细胞免受损伤。Hsp具有高度保守性,它们可能对于在潜在有害环境中的生存至关重要。大多数Hsp是分子伴侣,可感知未折叠蛋白并介导其重新折叠、转运和相互作用。在人类表皮中,Hsp与分化、光保护及皮肤病相关。近期研究主要集中于角质形成细胞中组成性表达的27kD和72kD Hsp。先前的热休克可抑制紫外线(UV)诱导的细胞死亡,并且UV本身可在实验中诱导Hsp。Hsp的调节可通过药理学方法进行修饰,目前正在研发Hsp表达的局部和全身诱导剂及抑制剂。光疗是否通过调节Hsp发挥其临床疗效尚未得到充分研究。干扰皮肤热休克反应所需的UV波长范围、强度和剂量仍有待阐明。

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