中文摘要：

光线性弹性组织变性的形成机制包括弹性纤维变性和堆积。弹性纤维的变性涉及活性氧簇增多、成纤维细胞的损伤和衰老、弹性蛋白酶和基质金属蛋白酶生成增加。堆积机制主要包括成纤维细胞合成弹性纤维增多、弹性蛋白分别与溶菌酶和皮肤来源的抗白细胞蛋白酶结合抵抗弹性蛋白酶降解、组织蛋白酶K活性降低等。组织蛋白酶K在光线性弹性组织变性堆积中的作用机制可能是未来研究光老化的新方向。

英文摘要：

The pathogenesis of solar elastosis consists of the degeneration and accumulation of elastic fibers. The degeneration of elastic fibers is related to increased reactive oxygen species, damage and aging of dermal fibroblasts and elevated production of elastase and matrix metalloproteinases. The accumulation of elastotic material is mainly associated with raised synthesis of elastic fibers, counteraction of elastic fibers combined with lysozymes and skin-derived antileukoprotease against elastase degradation, decreased activity of cathepsin K, etc. In the future, the action mechanism of cathepsin K in solar elastosis and elastotic material degradation may become a new focus in photoaging research.