Cutaneous Biology Research Center, Massachusetts General Hospital Department of Dermatology, Harvard Medical School, Boston, MA 02114, USA.
Cutaneous Biology Research Center, Massachusetts General Hospital Department of Dermatology, Harvard Medical School, Boston, MA 02114, USA.
Adv Drug Deliv Rev. 2020 Jan 1;153:65-71. doi: 10.1016/j.addr.2020.02.002. Epub 2020 Feb 21.
Skin pigmentation is a result of melanin produced by melanocytes in the epidermis. Melanocyte activity, along with the type and distribution of melanins, is the main driver for diversity of skin pigmentation. Dark melanin acts to protect against the deleterious effects of ultraviolet (UV) radiation, including photo-aging and skin cancer formation. In turn, UV radiation activates skin melanocytes to induce further pigmentation (i.e., "tanning pathway"). The well-characterized MSH/MC1R-cAMP-MITF pathway regulates UV-induced melanization. Pharmacologic activation of this pathway ("sunless tanning") represents a potential strategy for skin cancer prevention, particularly in those with light skin or the "red hair" phenotype who tan poorly after UV exposure due to MC1R inactivating polymorphisms. Skin hyperpigmentation can also occur as a result of inflammatory processes and dermatological disorders such as melasma. While primarily of cosmetic concern, these conditions can dramatically impact quality of life of affected patients. Several topical agents are utilized to treat skin pigmentation disorders. Here, we review melanogenesis induced by UV exposure and the agents that target this pathway.
皮肤色素沉着是由表皮中的黑素细胞产生的黑色素引起的。黑素细胞的活性以及黑色素的类型和分布是皮肤色素沉着多样性的主要驱动因素。深色黑色素可防止紫外线 (UV) 辐射的有害影响,包括光老化和皮肤癌的形成。反过来,UV 辐射会激活皮肤黑素细胞,诱导进一步的色素沉着(即“晒黑途径”)。特征明确的 MSH/MC1R-cAMP-MITF 途径调节 UV 诱导的黑色素形成。该途径的药理学激活(“非晒黑”)代表了预防皮肤癌的潜在策略,特别是对于那些皮肤白皙或“红发”表型的人,由于 MC1R 失活的多态性,他们在暴露于 UV 后晒黑效果不佳。皮肤色素沉着也可能是炎症过程和皮肤病如黄褐斑的结果。虽然主要是美容方面的问题,但这些情况会极大地影响受影响患者的生活质量。有几种局部药物可用于治疗皮肤色素沉着疾病。在这里,我们回顾了 UV 照射诱导的黑色素生成以及靶向该途径的药物。