Amano Satoshi
Shiseido Research Center, Yokohama, Kanagawa, Japan.
Exp Dermatol. 2016 Aug;25 Suppl 3:14-9. doi: 10.1111/exd.13085.
Sun-exposed skin is characterized by superficial changes such as wrinkles, sagging and pigmentary changes, and also many internal changes in the structure and function of epidermis, basement membrane (BM) and dermis. These changes (so-called photoageing) are predominantly induced by the ultraviolet (UV) component of sunlight. Epidermis of UV-irradiated skin produced several enzymes such as matrix metalloproteinases (MMPs), urinary plasminogen activator (uPA)/plasmin and heparanase, which degrade dermal collagen fibres and elastic fibres in the dermis, and components of epidermal BM. The BM at the dermal-epidermal junction (DEJ) controls dermal-epidermal signalling and plays an important role in the maintenance of a healthy epidermis and dermis. BM is repetitively damaged in sun-exposed skin compared with unexposed skin, leading to epidermal and dermal deterioration and accelerated skin ageing. UV exposure also induces an increase in vascular endothelial growth factor (VEGF), an angiogenic factor, while thrombospondin-1 (TSP-1), an anti-angiogenic factor, is decreased; these changes induce angiogenesis in papillary dermis with increased migration of elastase-positive leucocytes, leading to dermal elastic fibre damage. Elastic fibres, such as oxytalan fibres in papillary dermis, are associated with not only skin resilience, but also skin surface texture, and elastic fibre formation by fibroblasts is facilitated by increased expression of fibulin-5. Thus, induction of fibulin-5 expression is a damage-repair mechanism, and fibulin-5 is an early marker of photoaged skin. UV-induced skin damage is cumulative and leads to premature ageing of skin. However, appropriate daily skincare may ameliorate photoageing by inhibiting processes causing damage and enhancing repair processes.
暴露于阳光下的皮肤具有诸如皱纹、松弛和色素沉着变化等表面变化特征,同时在表皮、基底膜(BM)和真皮的结构和功能方面也存在许多内部变化。这些变化(所谓的光老化)主要由阳光中的紫外线(UV)成分引起。紫外线照射皮肤的表皮会产生几种酶,如基质金属蛋白酶(MMPs)、尿纤溶酶原激活剂(uPA)/纤溶酶和乙酰肝素酶,这些酶会降解真皮中的真皮胶原纤维和弹性纤维以及表皮BM的成分。真皮 - 表皮交界处(DEJ)的BM控制着真皮 - 表皮信号传导,在维持健康的表皮和真皮方面发挥着重要作用。与未暴露的皮肤相比,暴露于阳光下的皮肤中的BM会反复受损,导致表皮和真皮退化以及皮肤老化加速。紫外线照射还会诱导血管内皮生长因子(VEGF,一种血管生成因子)增加,而抗血管生成因子血小板反应蛋白 - 1(TSP - 1)减少;这些变化会诱导乳头真皮中的血管生成,同时弹性蛋白酶阳性白细胞的迁移增加,导致真皮弹性纤维损伤。弹性纤维,如乳头真皮中的氧化弹力纤维,不仅与皮肤弹性有关,还与皮肤表面质地有关,成纤维细胞对弹性纤维的形成会因纤连蛋白 - 5表达增加而得到促进。因此,诱导纤连蛋白 - 5表达是一种损伤修复机制,纤连蛋白 - 5是光老化皮肤的早期标志物。紫外线引起的皮肤损伤具有累积性,会导致皮肤过早老化。然而,适当的日常皮肤护理可以通过抑制造成损伤的过程并增强修复过程来改善光老化。