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SKIN AGING

  • Intrinsic aging: natural or chronologic aging, influenced by genetics

    • Begins in the mid-20s, but signs may not be visible for decades

    • Collagen production and cell turnover slows

    • Loss of subcutaneous fat and bone loss contribute to volume issues

  • Extrinsic aging: caused by environmental factors

    • Largest contributors are ultraviolet (UV) radiation (photoaging) and smoking

    • Facial expressions, sleeping positions, nutrition, and airborne particles (pollution) are additive factors

    • Solar elastosis or dermatoheliosis: term applied to the chronic inflammatory changes and degradation of elastin and collagen

OXIDATIVE STRESS (FREE RADICAL THEORY OF AGING)

  • Reactive oxygen species (ROS) derived from the environment and oxidative cell metabolism damage cellular components and lead to aging

    • Mitochondria are the main endogenous source of ROS

  • ROS activate signal transduction pathways including mitogen-activated protein kinases, c-jun N-terminal kinase (JNK), and extracellular signal related kinases, which upregulate the nuclear transcription factor activator protein 1 (AP-1)

  • AP-1 activates matrix metalloproteinase (MMP) genes for MMP-1 (collagenase), MMP-3 (stromolysin), and MMP-9 (gelatinase)

  • MMPs degrade collagen types I and III

  • AP-1 inhibits transforming growth factor B (TGF-B), a profibrotic cytokine, and downregulates type II TGF-B receptors so cells cannot respond to TGF-B and less type I procollagen is produced

  • Antioxidants such as vitamins A, C, and E, ubiquinone and glutathione may help to minimize ROS-induced damage

  • All-trans-retinoic acid (tretinoin) acts like an antioxidant to inhibit the accumulation of c-jun protein, thereby preventing the formation of AP-1 and the upregulation of MMPs

  • Tretinoin also induces TGF-B to enhance production of procollagen types I and III

Ultraviolet Radiation

  • UVA: 320 to 400 nm; largest contributor to Aging due to deeper penetration depth and ability to generate ROS

    • UVA1: 340 to 400 nm (longest wavelength and deepest penetration of all ultraviolet light)

    • UVA2: 320 to 340 nm

  • UVB: 290 to 320 nm; Burning rays; absorbed by the epidermis, mainly causing damage to keratinocytes in the form of pyrimidine dimers

    • Narrowband UVB: 311 to 312 nm

    • UVC: 100 to 290 nm; has negligible effect on skin as nearly all is blocked by the atmosphere

  • UVA rays make up 95% of UV radiation reaching the Earth's surface; however UVB rays are more intense

  • Both contribute to skin cancer, photoaging (wrinkles, discoloration, telangiectasias), and ocular changes (cataracts, pterygium)

  • UV radiation downregulates gene expression in types I and III procollagen in dermal fibroblasts

  • UV radiation activates transcription factor nuclear factor κB (NF-κB), resulting in transcription of proinflammatory cytokines such as IL-1β, tumor necrosis factor α, IL-6, and IL-8. Proinflammatory cytokines bind receptors on the cell surface to further activate AP-1 and NF-κB, escalating the photoaging response

  • Activation of MMP-1 and NF-κB are iron dependent mechanisms, so iron chelators such as kojic acid may be included in topical antiaging preparations

Telomeres and Aging

  • Telomeres form the ends of human chromosomes; defend the ends of chromosomes from instability

  • Comprised of repeats of ...

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