Krutmann Jean, Schroeder Peter
IUF, Duesseldorf, Germany.
J Investig Dermatol Symp Proc. 2009 Aug;14(1):44-9. doi: 10.1038/jidsymp.2009.1.
The exact pathogenesis of photoaging of the skin is not yet known. Earlier, a number of molecular pathways explaining one or more characteristics of photoaged skin have been described, but a unifying mechanistic concept is still missing. Here we propose the "Defective Powerhouse Model of Premature Skin Aging", which reconciles most of the earlier conducted research as one concept. In this model, the persistence of UV radiation-induced mtDNA deletions or the infrared radiation-induced disturbance of the electron flow of the mitochondrial electron transport chain leads to inadequate energy production in dermal fibroblasts. As a consequence of this defective powerhouse, retrograde mitochondrial signaling pathways are triggered that then they transduce functional and structural alterations in the skin. This model, which is supported by a growing number of recent studies, is of direct clinical importance in preventing and treating photoaging in human skin.Journal of Investigative Dermatology Symposium Proceedings (2009) 14, 44-49; doi:10.1038/jidsymp.2009.1.
皮肤光老化的确切发病机制尚不清楚。此前，已经描述了一些解释光老化皮肤一种或多种特征的分子途径，但仍缺乏一个统一的机制概念。在此，我们提出“皮肤过早老化的线粒体功能缺陷模型”，该模型将此前的大多数研究统一为一个概念。在这个模型中，紫外线辐射诱导的线粒体DNA缺失持续存在，或红外线辐射引起的线粒体电子传递链电子流紊乱，导致真皮成纤维细胞能量产生不足。由于这种线粒体功能缺陷，逆行线粒体信号通路被触发，进而导致皮肤发生功能和结构改变。这个模型得到了越来越多近期研究的支持，对预防和治疗人类皮肤光老化具有直接的临床意义。《皮肤病学研究杂志研讨会论文集》（2009年）14卷，44 - 49页；doi:10.1038/jidsymp.2009.1
