Papaccio Federica, D Arino Andrea, Caputo Silvia, Bellei Barbara
Laboratory of Cutaneous Physiopathology and Integrated Center of Metabolomics Research, San Gallicano Dermatological Institute, IRCCS, 00144 Rome, Italy.
Antioxidants (Basel). 2022 Jun 6;11(6):1121. doi: 10.3390/antiox11061121.
Skin aging is one of the most evident signs of human aging. Modification of the skin during the life span is characterized by fine lines and wrinkling, loss of elasticity and volume, laxity, rough-textured appearance, and pallor. In contrast, photoaged skin is associated with uneven pigmentation (age spot) and is markedly wrinkled. At the cellular and molecular level, it consists of multiple interconnected processes based on biochemical reactions, genetic programs, and occurrence of external stimulation. The principal cellular perturbation in the skin driving senescence is the alteration of oxidative balance. In chronological aging, reactive oxygen species (ROS) are produced mainly through cellular oxidative metabolism during adenosine triphosphate (ATP) generation from glucose and mitochondrial dysfunction, whereas in extrinsic aging, loss of redox equilibrium is caused by environmental factors, such as ultraviolet radiation, pollution, cigarette smoking, and inadequate nutrition. During the aging process, oxidative stress is attributed to both augmented ROS production and reduced levels of enzymatic and non-enzymatic protectors. Apart from the evident appearance of structural change, throughout aging, the skin gradually loses its natural functional characteristics and regenerative potential. With aging, the skin immune system also undergoes functional senescence manifested as a reduced ability to counteract infections and augmented frequency of autoimmune and neoplastic diseases. This review proposes an update on the role of oxidative stress in the appearance of the clinical manifestation of skin aging, as well as of the molecular mechanisms that underline this natural phenomenon sometimes accelerated by external factors.
皮肤老化是人类衰老最明显的迹象之一。在整个生命周期中，皮肤的变化特征为出现细纹和皱纹、弹性和体积丧失、松弛、质地粗糙以及面色苍白。相比之下，光老化皮肤与色素沉着不均（老年斑）有关，且皱纹明显。在细胞和分子水平上，它由基于生化反应、遗传程序和外部刺激发生的多个相互关联的过程组成。皮肤中驱动衰老的主要细胞扰动是氧化平衡的改变。在自然老化过程中，活性氧（ROS）主要通过葡萄糖生成三磷酸腺苷（ATP）期间的细胞氧化代谢以及线粒体功能障碍产生，而在外源性老化过程中，氧化还原平衡的丧失是由环境因素引起的，如紫外线辐射、污染、吸烟和营养不足。在衰老过程中，氧化应激归因于ROS生成增加以及酶性和非酶性保护剂水平降低。除了明显的结构变化外，在整个衰老过程中，皮肤逐渐失去其天然功能特性和再生潜力。随着年龄增长，皮肤免疫系统也会经历功能衰老，表现为抵抗感染的能力下降以及自身免疫性疾病和肿瘤疾病的发病率增加。本综述对氧化应激在皮肤老化临床表现出现中的作用以及这种有时由外部因素加速的自然现象背后的分子机制进行了更新。
