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探索皮肤衰老的机制:为临床治疗提供的见解。

Exploring mechanisms of skin aging: insights for clinical treatment.

机构信息

School of Medical and Life Sciences, Chengdu University of Traditional Chinese Medicine, Chengdu, China.

Health Management Center, Nanjing Tongren Hospital, School of Medicine, Southeast University, Nanjing, China.

出版信息

Front Immunol. 2024 Nov 8;15:1421858. doi: 10.3389/fimmu.2024.1421858. eCollection 2024.

Abstract

The skin is the largest organ in the human body and is made up of various cells and structures. Over time, the skin will age, which is not only influenced by internal factors, but also by external environmental factors, especially ultraviolet radiation. Aging causes immune system weakening in the elderly, which makes them more susceptible to dermatosis, such as type 2 inflammatory mediated pruritus. The immune response in this condition is marked by senescent cells consistently releasing low amounts of pro-inflammatory cytokines through a senescence-associated secretory phenotype (SASP). This continuous inflammation may accelerate immune system aging and establish a connection between immune aging and type 2 inflammatory skin diseases. In addition, two chronic pigmentation disorders, vitiligo and chloasma, are also associated with skin aging. Aged cells escape the immune system and accumulate in tissues, forming a microenvironment that promotes cancer. At the same time, "photoaging" caused by excessive exposure to ultraviolet radiation is also an important cause of skin cancer. This manuscript describes the possible links between skin aging and type 2 inflammation, chronic pigmentation disorders, and skin cancer and suggests some treatment options.

摘要

皮肤是人体最大的器官,由各种细胞和结构组成。随着时间的推移,皮肤会衰老,这不仅受内部因素的影响,还受外部环境因素的影响,特别是紫外线辐射。衰老使老年人的免疫系统减弱,使他们更容易患上皮肤病,如 2 型炎症介导的瘙痒症。这种情况下的免疫反应的特点是衰老细胞通过衰老相关分泌表型(SASP)持续释放少量促炎细胞因子。这种持续的炎症可能会加速免疫系统的衰老,并在免疫衰老和 2 型炎症性皮肤病之间建立联系。此外,两种慢性色素沉着障碍,白癜风和黄褐斑,也与皮肤衰老有关。衰老细胞逃避免疫系统并在组织中积累,形成促进癌症的微环境。同时,过度暴露于紫外线辐射引起的“光老化”也是皮肤癌的重要原因。本文描述了皮肤衰老与 2 型炎症、慢性色素沉着障碍和皮肤癌之间可能存在的联系,并提出了一些治疗选择。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acd7/11581952/99a253de6cbb/fimmu-15-1421858-g001.jpg

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