Abstract：
Telomeres, the safeguarding caps at the tips of chromosomes, are pivotal in the aging process of cells and have been linked to skin ailments and inflammatory conditions. Telomeres undergo a gradual reduction in length and factors such as oxidative stress hasten this diminishing process. Skin diseases including inflammatory conditions can be correlated with the shortening of telomeres and the persistent activation of DNA damage response in skin tissues. Telomere dysfunction could disrupt the balance of the skin, impairs wound healing, and may contribute to abnormal cytokine production. Skin aging and processes related to telomeres may function as one of the triggers for skin diseases. The presence of proinflammatory cytokines and dysfunctional telomeres in conditions such as Dyskeratosis Congenita implies a possible connection between the shortening of telomeres and the onset of chronic inflammatory skin disorders. In autoinflammatory skin diseases, chronic inflammation hinders wound healing thus aggravating the progression of the disease. The NF-ĸB pathway might contribute to the initiation or progression of chronic disorders by influencing mechanisms associated with telomere biology. The intricate connections between telomeres, telomerase, telomere-associated proteins, and skin diseases are still a complex puzzle to be solved. Here, we provide an overview of the impact of telomeres on both health and disease with a specific emphasis on their role in skin, inflammation and autoinflammatory skin disorders.
摘要：
端粒,染色体顶端的保护帽，在细胞衰老过程中至关重要，并与皮肤疾病和炎症有关。端粒的长度逐渐减少，氧化应激等因素加速了这种减少的过程。包括炎性病症的皮肤病可与皮肤组织中端粒的缩短和DNA损伤应答的持续激活相关。端粒功能障碍会破坏皮肤的平衡,损害伤口愈合，并可能导致细胞因子的异常产生。皮肤老化和与端粒相关的过程可能是皮肤病的触发因素之一。促炎细胞因子和功能失调的端粒在诸如先天性角化病的病症中的存在暗示端粒的缩短与慢性炎性皮肤病的发作之间的可能联系。在自身炎症性皮肤病中，慢性炎症阻碍伤口愈合，从而加重疾病的进展。NF-κB通路可能通过影响与端粒生物学相关的机制来促进慢性疾病的发生或发展。端粒之间错综复杂的联系，端粒酶,端粒相关蛋白，皮肤病仍然是一个需要解决的复杂难题。这里,我们概述了端粒对健康和疾病的影响，特别强调它们在皮肤中的作用，炎症和自身炎症性皮肤病。
