瘢痕疙瘩形成中机械力和炎症免疫相互作用的研究进展
Advances in the interplay between mechanical forces and inflammatory immunity in keloid formation.
摘要(中文译文)
瘢痕疙瘩是一种慢性炎症性纤维增殖性疾病，以超越原始创面边界的侵袭性生长和高复发率为特征，严重影响患者的生活质量。其发病机制复杂，由机械微环境、慢性炎症与促纤维化信号网络之间的协同交互作用所驱动。正常创面愈合的炎症期和增殖期发生病理性延长，成纤维细胞和肌成纤维细胞持续活化，导致细胞外基质（ECM）过度沉积和异常重塑。在免疫微环境中，浸润的M2型巨噬细胞及Th2/Th17细胞等分泌大量细胞因子，从而建立慢性炎症环路。机械力是关键驱动因素：高张力区域的应力集中以及成纤维细胞机械转导通路（如Hippo-YAP/TAZ和整合素-FAK）的激活与炎症反应相互作用，形成自我放大的“机械力-炎症-纤维化”正反馈环路，加剧疾病进展。当前治疗主要依赖手术联合放疗、病灶内药物注射等多模式方案，但仍面临高复发率和显著异质性的挑战。近年来，基于机械调控的减张方法以及针对JAK/STAT、IL-4/IL-13等炎症通路的靶向治疗已取得进展，整合“力学-炎症”的联合干预正成为新的方向。本文综述了瘢痕疙瘩的病理生理特征，阐明了机械力与炎症的作用及交互对话，从而为未来瘢痕疙瘩的个体化临床管理提供了以机械免疫学为核心的新理论框架。
Abstract
Keloids are chronic inflammatory fibroproliferative disorders characterized by invasive growth beyond the original wound margins and a high recurrence rate, substantially impairing patients' quality of life. Their pathogenesis is complex and arises from the synergistic interplay among the mechanical microenvironment, chronic inflammation, and profibrotic signaling networks. The inflammatory and proliferative phases of normal wound healing are pathologically prolonged, with sustained activation of fibroblasts and myofibroblasts, resulting in excessive extracellular matrix (ECM) deposition and aberrant remodeling. Within the immune microenvironment, infiltrating M2 macrophages and Th2/Th17 cells, among others, secrete a broad array of cytokines, thereby establishing a chronic inflammatory circuit. Mechanical forces act as a pivotal driving factor: stress concentration in high-tension regions and activation of fibroblast mechanotransduction pathways (e.g., Hippo-YAP/TAZ and integrin-FAK) interact with inflammatory responses to form a self-amplifying "mechanical force-inflammation-fibrosis" positive feedback loop, exacerbating disease progression. Current management primarily relies on multimodal regimens such as surgery combined with radiotherapy and intralesional pharmacologic injections, yet remains challenged by high recurrence rates and marked heterogeneity. In recent years, tension-reduction approaches grounded in mechanomodulation and targeted therapies against inflammatory pathways such as JAK/STAT and IL-4/IL-13 have shown progress, and integrated "mechanics-inflammation" combinatorial interventions are emerging as a new direction. The review summarizes the pathophysiological features of keloids and elucidates the roles and crosstalk of mechanical forces and inflammation, thereby providing a novel theoretical framework centered on mechano-immunology for future individualized clinical management of keloids.
如何引用
AMA
Simin Zhou, Lei Wang, Nannan Chen, Jinqiao Liu, Rongjia Zhang, Shiqi Zhou, et al. Advances in the interplay between mechanical forces and inflammatory immunity in keloid formation.. Frontiers in immunology. 2026; doi:10.3389/fimmu.2026.1792028.
APA
Simin Zhou, Lei Wang, Nannan Chen, Jinqiao Liu, Rongjia Zhang, Shiqi Zhou, et al (2026). Advances in the interplay between mechanical forces and inflammatory immunity in keloid formation.. Frontiers in immunology. https://doi.org/10.3389/fimmu.2026.1792028
GB/T 7714
Simin Zhou, Lei Wang, Nannan Chen, Jinqiao Liu, Rongjia Zhang, Shiqi Zhou, et al. Advances in the interplay between mechanical forces and inflammatory immunity in keloid formation.[J]. Frontiers in immunology, 2026 doi:10.3389/fimmu.2026.1792028.
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