Andrzejczak Klara, Sternak Agata, Witkowski Wiktor, Ponikowska Małgorzata
Faculty of Medicine, Wroclaw Medical University, Wybrzeze L. Pasteura 1, 50-367 Wroclaw, Poland.
Student Research Group of Experimental Dermatology, University Centre of General Dermatology and Oncodermatology, Wroclaw Medical University, 50-556 Wroclaw, Poland.
Cells. 2025 Sep 15;14(18):1442. doi: 10.3390/cells14181442.
Chronic inflammatory skin diseases such as atopic dermatitis, psoriasis, and hidradenitis suppurativa are systemic conditions marked by persistent immune activation. Growing evidence links them to molecular and vascular ageing, including oxidative stress, endothelial dysfunction, and reduced expression of longevity-related proteins like Klotho and SIRT1. This narrative review examines how Th17- and Th2-driven inflammation contributes to systemic inflammageing. Key cytokines-IL-17, IL-23, IL-4, IL-13, and IL-31-promote endothelial damage, oxidative stress, and metabolic dysfunction. We highlight the role of vascular biomarkers (e.g., VCAM-1, ICAM-1, ST2, P-selectin) and immune cell senescence as indicators of ageing. Finally, we explore whether biologic therapies targeting these pathways may attenuate inflammation-driven ageing. Chronic skin diseases may thus serve as accessible models of systemic inflammageing and targets for early intervention.
特应性皮炎、银屑病和化脓性汗腺炎等慢性炎症性皮肤病是由持续免疫激活所标记的全身性疾病。越来越多的证据将它们与分子和血管衰老联系起来，包括氧化应激、内皮功能障碍以及诸如Klotho和SIRT1等长寿相关蛋白表达的降低。这篇叙述性综述探讨了由Th17和Th2驱动的炎症如何导致全身性炎症衰老。关键细胞因子——白细胞介素-17、白细胞介素-23、白细胞介素-4、白细胞介素-13和白细胞介素-31——促进内皮损伤、氧化应激和代谢功能障碍。我们强调血管生物标志物（如血管细胞黏附分子-1、细胞间黏附分子-1、ST2、P-选择素）和免疫细胞衰老作为衰老指标的作用。最后，我们探讨针对这些途径的生物疗法是否可能减轻炎症驱动的衰老。因此，慢性皮肤病可能成为全身性炎症衰老的易获取模型和早期干预的靶点。
