玫瑰痤疮的发病机制的研究进展
Research Progress on the Pathogenesis of Rosacea
DOI: 10.12677/acm.2026.1641637, PDF,   
作者: 谢天华, 高 奥, 胡云峰*：暨南大学附属第一医院皮肤科，广东 广州；郝 晋：河北中医药大学中西医结合学院，河北 石家庄
关键词: 玫瑰痤疮；免疫机制；神经–血管调节；TRPV受体；TLR受体；mTORC1信号通路；肥大细胞；Rosacea； Immune Mechanisms； Neurovascular Regulation； TRPV Receptors； TLR Receptors； mTORC1 Signaling Pathway； Mast Cells
摘要: 玫瑰痤疮是一种以面部慢性炎症为特征的皮肤疾病，其发病机制尚未完全明确。近年来研究表明，固有免疫异常激活、获得性免疫反应参与以及炎症因子网络失衡在疾病发生发展中发挥重要作用，其中TLR2-LL-37-mTORC1轴、JAK-STAT信号通路及NLRP3炎性小体等通路尤为关键。此外，补体系统及Toll样受体通路的调控异常亦参与炎症放大过程。本文综述玫瑰痤疮相关免疫炎症机制及其分子通路，为疾病的靶向治疗和个体化干预提供理论依据。
Abstract: Rosacea is a skin disease characterized by chronic facial inflammation, and its pathogenesis is not yet fully understood. Recent studies have shown that abnormalities in innate immune activation, involvement of adaptive immune responses, and imbalance in inflammatory factor networks play crucial roles in the development of the disease. Among these, the TLR2-LL-37-mTORC1 axis, JAK-STAT signaling pathway, and NLRP3 inflammasome are particularly important. Additionally, dysregulation of the complement system and Toll-like receptor pathways also contribute to the amplification of inflammation. This review summarizes the immune-inflammatory mechanisms and molecular pathways involved in rosacea, providing a theoretical basis for targeted treatment and personalized intervention.
文章引用：谢天华, 高奥, 郝晋, 胡云峰. 玫瑰痤疮的发病机制的研究进展[J]. 临床医学进展, 2026, 16(4): 3725-3730. https://doi.org/10.12677/acm.2026.1641637

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