摘要
人类皮肤老化分为内源性和外源性两种,紫外线辐射是外源性老化的最主要因素,所以又称为光老化。细胞染色体末端的特殊结构———端粒,在皮肤老化过程中扮演了非常重要的角色。细胞多次分裂造成的端粒进行性缩短很大程度上控制了内源性老化。暴露于日光的皮肤,紫外线辐射也可损伤DNA,加速端粒缩短。无论是内源性老化还是光老化,在端粒环破裂后均通过p 53肿瘤抑制蛋白途径启动了DNA损伤信号传递。这一共同的路径解释了自然老化和光老化皮肤的广泛相似性,预示着对一种老化进程采取有效的预防和治疗措施可能对其他进程产生良性影响。
There are two primary skin aging processes, intrinsic and extrinsic. This latter process is due mainly to ultraviolet (UV) irradiation and is termed photoaging. Telomeres, the specialized structures found at the ends of chromosomes, play an essential role in both of the skin aging processes. Intrinsic aging is largely controlled by progressive telomere shortening, the consequence of serial cell division. In sun - exposed skin, UV irradiation also damages DNA and accelerates telomere shortening. Both intrinsic skin aging and photoaging appear to share a common final pathway that involves signaling through p53 following disruption of the telomere loop. This postulated mechanistic overlap explains the extensive: similarities between aged and photoaged skin and predicts that preventive or therapeutic strategies effective in one process might well impact the other as well.
出处
《中国皮肤性病学杂志》
CAS
北大核心
2009年第5期313-315,共3页
The Chinese Journal of Dermatovenereology
关键词
端粒
端粒酶
皮肤老化
Telomeres
Telomerase
Skin aging