光老化是一个复杂的、持续的过程，临床上表现为皮肤皱纹、萎缩、松弛、色素沉着、毛细血管扩张、粗糙和皮肤出现斑点。有大量研究建立了紫外线 (UV) 引起的光损伤的机制，因为它是光老化和皮肤癌的重要来源。虽然已知紫外线损伤会引起光老化，但了解其他形式的光辐射如何促进这一过程也很重要。到达地球表面的太阳辐射中，紫外线仅占 5% 至 10%。剩余的近 90% 均匀分布在红外光和可见光辐射之间。早期研究表明，不同的皮肤类型可能会对光产生不同的光生物学反应。本文介绍了跨光谱光（包括紫外线、可见光和红外线）引起的光损伤的机制和生物标志物，以更好地预防和逆转所有皮肤类型的光老化损伤。J Drugs Dermatol。 2024；23(7):504-509。

Photoaging is a complex, ongoing process that clinically manifests as cutaneous rhytides, atrophy, laxity, dyspigmentation, telangiectasias, roughness, and mottled appearance of the skin. There is an abundance of research establishing the mechanism of ultraviolet (UV) - induced photodamage as it is a significant source of photoaging and skin cancers. While UV damage is known to induce photoaging, it is important to understand how other forms of light radiation also contribute to this process. UV only constitutes 5 to 10% of solar radiation that reaches the earth's surface. The remaining nearly 90% is evenly split between infrared and visible light radiation. Early research shows that varied skin types may elicit different photobiologic responses to light. This article presents the mechanisms and biomarkers of photodamage induced by light from across the spectrum, including UV, visible light, and infrared to better prevent and reverse the damage of photoaging in all skin types.J Drugs Dermatol. 2024;23(7):504-509.  doi:10.36849/JDD.7438.