Department of Ophthalmology, Taipei Veterans General Hospital, Taipei 112, Taiwan.
Office of Business Development, Technology Commercialization Center, Taipei Medical University, Taipei 110, Taiwan.
Cells. 2024 Sep 5;13(17):1493. doi: 10.3390/cells13171493.
TGF-β plays a pivotal role in the pathogenesis of GO by promoting orbital tissue remodeling and fibrosis. This process involves the stimulation of orbital fibroblasts, leading to myofibroblast differentiation, increased production of inflammatory mediators, and hyaluronan accumulation. Studies have elucidated TGF-β's role in driving fibrosis and scarring processes through both canonical and non-canonical pathways, particularly resulting in the activation of orbital myofibroblasts and the excessive accumulation of extracellular matrix. Additionally, recent in vitro and in vivo studies have been summarized, highlighting the therapeutic potential of targeting TGF-β signaling pathways, which may offer promising treatment interventions for GO. This review aims to consolidate the current understanding of the multifaceted role of TGF-β in the molecular and cellular pathophysiology in Graves' ophthalmopathy (GO) by exploring its contributions to fibrosis, inflammation, and immune dysregulation. Additionally, the review investigates the therapeutic potential of inhibiting TGF-β signaling pathways as a strategy for treating GO.
TGF-β 在 GO 的发病机制中发挥关键作用，通过促进眼眶组织重塑和纤维化。这个过程涉及到眼眶成纤维细胞的刺激，导致肌成纤维细胞分化，炎症介质的产生增加，以及透明质酸的积累。研究已经阐明了 TGF-β 通过经典和非经典途径驱动纤维化和瘢痕形成过程的作用，特别是导致眼眶肌成纤维细胞的激活和细胞外基质的过度积累。此外，最近的体外和体内研究已经被总结，强调了靶向 TGF-β 信号通路的治疗潜力，这可能为 GO 提供有前途的治疗干预措施。本综述旨在通过探讨 TGF-β 在格雷夫斯眼病（GO）的分子和细胞病理生理学中的多方面作用，来整合目前对 TGF-β 的理解，即探讨其在纤维化、炎症和免疫失调中的作用。此外，本综述还研究了抑制 TGF-β 信号通路作为治疗 GO 的一种策略的治疗潜力。
