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光老化和自然皮肤老化的机制。

Mechanisms of photoaging and chronological skin aging.

作者信息

Fisher Gary J, Kang Sewon, Varani James, Bata-Csorgo Zsuzsanna, Wan Yinsheng, Datta Subhash, Voorhees John J

机构信息

Department of Dermatology, University of Michigan, Ann Arbor, MI 48109, USA.

出版信息

Arch Dermatol. 2002 Nov;138(11):1462-70. doi: 10.1001/archderm.138.11.1462.

Abstract

Human skin, like all other organs, undergoes chronological aging. In addition, unlike other organs, skin is in direct contact with the environment and therefore undergoes aging as a consequence of environmental damage. The primary environmental factor that causes human skin aging is UV irradiation from the sun. This sun-induced skin aging (photoaging), like chronological aging, is a cumulative process. However, unlike chronological aging, which depends on the passage of time per se, photoaging depends primarily on the degree of sun exposure and skin pigment. Individuals who have outdoor lifestyles, live in sunny climates, and are lightly pigmented will experience the greatest degree of photoaging. During the last decade, substantial progress has been made in understanding cellular and molecular mechanisms that bring about chronological aging and photoaging. This emerging information reveals that chronological aging and photoaging share fundamental molecular pathways. These new insights regarding convergence of the molecular basis of chronological aging and photoaging provide exciting new opportunities for the development of new anti-aging therapies. This article reviews our current understanding and presents new data about the molecular pathways that mediate skin damage by UV irradiation and by the passage of time.

摘要

和所有其他器官一样,人类皮肤会经历自然老化。此外,与其他器官不同的是,皮肤直接与环境接触,因此会因环境损伤而老化。导致人类皮肤老化的主要环境因素是太阳的紫外线辐射。这种由阳光引起的皮肤老化(光老化),与自然老化一样,是一个累积的过程。然而,与主要取决于时间本身流逝的自然老化不同,光老化主要取决于阳光照射程度和皮肤色素。有户外生活方式、生活在阳光充足气候地区且色素较浅的人会经历最严重的光老化。在过去十年中,在理解导致自然老化和光老化的细胞和分子机制方面取得了重大进展。这些新出现的信息表明,自然老化和光老化共享基本的分子途径。这些关于自然老化和光老化分子基础趋同的新见解为开发新的抗衰老疗法提供了令人兴奋的新机会。本文综述了我们目前的理解,并展示了关于紫外线辐射和时间推移介导皮肤损伤的分子途径的新数据。

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