利益冲突声明

您有否接受任何资金来支持研究这个主题？
否

您是否接受过关于这项研究的任何酬金或其他报酬？
是
请注明名称（个人，公司，学会等等）: Not specifically for this topic, but have participated in round table on this topic sponsored by SkinCeuticals in 2016

你是否和任何与您的研究所涉及的药物，材料或工具有密切联系的实体存在财务关系？
否

你是否拥有或者您已经为您此研究中的工具，药物或材料申请任何专利？
否

这项工作没有任何直接或间接的资金支持。由作者自己承担责任。

Objectives: To examine how the amount, subtype and distribution of melanin in skin can affect how the skin photoages.

Introduction: Casual comparison of the appearance and texture of unprotected photo-exposed hand and face skin versus skin of the secluded body sites reveals a striking impact of accumulated solar radiation on skin aging, particularly after the 3rd or 4th decades of life. The basis of this change is revealed in anatomical, histological, and ultrastructural changes in the epidermis and dermis of the skin, which result from alterations at the cellular and molecular levels. Principal among these is the marked flattening of the dermal-epidermal junction with consequent loss of rete ridges.

Materials / method: Examination of skin from normal healthy individuals of different ages and comparison to conditions with pigment loss (e.g., vitiligo) at tissue, protein and cell culture levels.

Results: Actinic skin aging-associated changes remains largely unexplained in terms of mechanism, but are underpinned by key interactions between functional units in the skin, including the epidermal-melanin- and epidermal-dermal cell-units. Some of these solar-light driven changes involve phenotype switching in dermal fibroblasts, including via their adoption of senescent phenotype with associated dysfunctional secretomes. There is increasing evidence that environmental pollution and even certain wavelengths of visible light can also contribute to the global ‘photo-aging’ response.

Conclusion: Human skin is equipped at least partially with effective protective devices against actinic damage; principal among them includes the synthesis of copious amounts melanin that acts as a near-universal stress absorber. This enigmatic indole biopolymer acts as a ‘sink’ for toxins, pollutants, drugs, as well as a redox buffer against a host of reactive oxygen species. Brown/black (or wild-type) melanin far outperforms the photo-labile red/yellow pheomelanin, which increases the vulnerability of the of the skin to photo-damage and so photo-carcinogenesis.

利益冲突声明

您有否接受任何资金来支持研究这个主题？
是
请注明名称（个人，公司，学会等等）: Unilever, Procter & Gamble, LVMH, Boots

您是否接受过关于这项研究的任何酬金或其他报酬？
否

你是否和任何与您的研究所涉及的药物，材料或工具有密切联系的实体存在财务关系？
否

你是否拥有或者您已经为您此研究中的工具，药物或材料申请任何专利？
否

这项工作没有任何直接或间接的资金支持。由作者自己承担责任。

Objectives: Cellular mechanisms involved in pollution induced skin damage with special focus on ozone

Introduction: Atmospheric factors such as air pollution (smog, ozone, particulate matter, etc.) have been implicated in premature skin aging and possibly being associated with skin pathologies. Among the pollutants to which cutaneous tissue is exposed, ozone has been shown to be one of the most noxious. The skin damage caused by ozone exposure is largely attributable to a complex cascade of reactions in the skin initiated by the generation of reactive oxygen species (ROS), which causes oxidative damage to cellular components such as proteins, lipids and nucleic acids.

Conclusion: The damaged skin cells initiate inflammatory responses leading to the eventual damage manifested in chronically exposed skin. ROS generation and increased inflammatory mediators leads to positive feedback, named “OxInflammation”, that can further augment the skin damage.

利益冲突声明

您有否接受任何资金来支持研究这个主题？
是
请注明名称（个人，公司，学会等等）: SkinCeuticals

您是否接受过关于这项研究的任何酬金或其他报酬？
否

你是否和任何与您的研究所涉及的药物，材料或工具有密切联系的实体存在财务关系？
是
请注明名称（个人，公司，学会等等）: SkinCeuticals

你是否拥有或者您已经为您此研究中的工具，药物或材料申请任何专利？
否

这项工作没有任何直接或间接的资金支持。由作者自己承担责任。

Objectives: To determine if epigenetics reflects the degree to which skin has aged due to intrinsic and extrinsic factors.
Secondly, to determine if weekly or monthly sun-exposure leads to epigenetic drift, and whether sun-protection factor (SPF) creams can negate such drift.

Introduction: Lifestyles have a strong influence on the way we age. For example, combinations of lifestyle factors have been linked to looking 10 years younger, and influence ageing through their effect on epigenetics – these are DNA and histones modifications that control the activity of genes in our cells. As we age, however, epigenetic drift occurs, disrupting normal gene activity. In addition, the concept of an epigenetic clock is rapidly gaining popularity within ageing research, but its relevance to intrinsic and extrinsic skin ageing is unclear.

Materials / method: We carried out 3 epigenetic studies:
A) A cross-sectional biopsy study involving 24 Chinese and 24 Caucasian young and old female participants.
B) A longitudinal biopsy study involving 60 females. Subjects applied a SPF product to one arm over five months, tracked with instrumental measures, and biopsies taken from both arms at baseline and at the end of the study.
C) Ex-vivo skin study using 1-week repeat UV exposure for epigenetic drift and protection thereof by SPF products.
Methylation levels were tested on extracted DNA from biopsies and ex-vivo skin.

Results: We used the cross-sectional study along with complementary published studies to generate an intrinsic and extrinsic skin clock and show they detect differences in the rate of ageing in sun-exposed and sun-protected skin. For the longitudinal 5-month study, incidental, short-term sun-exposure led to a significant epigenetic drift and in the direction expected by chronic sun-damage; SPF product-use significantly reduced the drift. An almost identical epigenetic drift and SPF protection were detected in the ex-vivo models.

Conclusion: The degree that skin had aged was captured by both an intrinsic and extrinsic skin clock, and we are the first to demonstrate that UV-induced epigenetic drift occurs even during incidental, short-term sun-exposure. SPF products can significantly reduce the drift, reinforcing the importance of daily sun-protection.

利益冲突声明

您有否接受任何资金来支持研究这个主题？
是
请注明名称（个人，公司，学会等等）: Unilever

您是否接受过关于这项研究的任何酬金或其他报酬？
是
请注明名称（个人，公司，学会等等）: Unilever

你是否和任何与您的研究所涉及的药物，材料或工具有密切联系的实体存在财务关系？
是
请注明名称（个人，公司，学会等等）: I'm a Unilever employee

你是否拥有或者您已经为您此研究中的工具，药物或材料申请任何专利？
是
请注明日期: Submitted
和审阅情况: 2018

这项工作的完成感谢以下机构的支持： Unilever