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Skin appearance and functionality are affected by a complex combination of factors including both genetic, i.e. intrinsic, and actinic, i.e. extrinsic or environmental. Indeed, genetic and actinic factors act together to modulate the expression of key genes involved in skin homeostasis. Intrinsic aging is genetically regulated and follows a chronological clock inside of cells, while environmental factors such as UV exposure, humidity and air pollutants are responsible for actinic aging. Together, genetic and actinic aging target important metabolic pathways in skin cells that trigger the signs of aging such as skin roughness and wrinkling.
At a molecular level, it has been demonstrated that collagen synthesis is reduced in aged skin cells and in cells damaged by UV radiation.1 Similarly, the expression of various matrix metalloproteases (MMPs), which cause the degradation of collagen fibers and other skin fibrillar components, is upregulated in aged cells as well as in cells exposed to UV, infrared radiation or excessive heat.2, 3 Furthermore, reactive oxygen species are molecular agents implicated in the deleterious effects of both intrinsic and extrinsic aging.1, 4
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