通过激活 NF-κB 参与血栓闭塞性脉管炎发病机制的 Toll 样受体信号通路

IF 2.2 4区 医学 Q2 MEDICINE, GENERAL & INTERNAL Clinics Pub Date : 2024-01-01 DOI:10.1016/j.clinsp.2024.100357
Facai Guo , Yan Bi , Jiangyan Yin , Yi Guo
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引用次数: 0

摘要

目的血栓闭塞性脉管炎(TAO)的发病机制尚不完全清楚,而自身免疫性炎症在TAO活动的开始和持续中起着至关重要的作用。作者在本研究中探讨了 TLR 信号通路在 TAO 发病机制中的作用。方法首先,作者通过 Western 印迹检测了 46 名 TAO 患者和 32 名外伤及骨肉瘤患者血管壁中 MyD88、TRIF 和 NF-κB 的表达。其次,作者通过免疫荧光法检测了MyD88、TRIF和NF-κB在TAO患者血管壁中的细胞定位。在 TAO 患者的血管内皮细胞和血管平滑肌细胞中均检测到 MyD88 和 NF-κB 的较高表达。结论 这些研究结果表明,TLR信号通路可能在TAO的发病机制中发挥重要作用,它可能诱导血管痉挛、血管炎和血栓形成,从而导致TAO的发病和进展。
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Toll-like receptor signaling pathway involved in pathogenesis of thromboangiitis obliterans through activating of NF-κB

Objectives

The pathogenic mechanisms of Thromboangiitis Obliterans (TAO) are not entirely known and autoimmune inflammation plays a vital role in the initiation and continuance of TAO activity. The authors investigated in this study the role of the TLR signaling pathway in the pathogenesis of TAO.

Methods

First, the authors detected the expressions of MyD88, TRIF and NF-κB in vascular walls of 46 patients with TAO and 32 patients with trauma and osteosarcoma by western blot assay. Second, the authors detected the cellular localization of MyD88, TRIF and NF-κB in vascular walls of patients with TAO by immunofluorescent assay.

Results

The protein expressions of MyD88, TRIF and NF-κB were much higher in vascular walls of TAO patients (p < 0.05). Higher expressions of MyD88 and NF-κB were detected both on vascular endothelial and vascular smooth muscle cells of TAO patients. However, higher expression of TRIF was just detected on vascular smooth muscle cells of TAO patients.

Conclusions

These dates suggest that the TLR signaling pathway might play an important role in the pathogenesis of TAO, it might induce vasospasm, vasculitis and thrombogenesis to lead to the pathogenesis and progression of TAO.

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来源期刊
Clinics
Clinics 医学-医学:内科
CiteScore
4.10
自引率
3.70%
发文量
129
审稿时长
52 days
期刊介绍: CLINICS is an electronic journal that publishes peer-reviewed articles in continuous flow, of interest to clinicians and researchers in the medical sciences. CLINICS complies with the policies of funding agencies which request or require deposition of the published articles that they fund into publicly available databases. CLINICS supports the position of the International Committee of Medical Journal Editors (ICMJE) on trial registration.
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