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基于生物材料的脊髓损伤修复策略:TLR4-NF-κB信号通路

Strategies for Biomaterial-Based Spinal Cord Injury Repair the TLR4-NF-κB Signaling Pathway.

作者信息

Lv Bin, Shen Naiting, Cheng Zhangrong, Chen Yuhang, Ding Hua, Yuan Jishan, Zhao Kangchen, Zhang Yukun

机构信息

Department of Orthopaedics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

出版信息

Front Bioeng Biotechnol. 2022 Apr 29;9:813169. doi: 10.3389/fbioe.2021.813169. eCollection 2021.

Abstract

The repair and motor functional recovery after spinal cord injury (SCI) has remained a clinical challenge. Injury-induced gliosis and inflammation lead to a physical barrier and an extremely inhibitory microenvironment, which in turn hinders the recovery of SCI. TLR4-NF-κB is a classic implant-related innate immunomodulation signaling pathway and part of numerous biomaterial-based treatment strategies for SCI. Numerous experimental studies have demonstrated that the regulation of TLR4-NF-κB signaling pathway plays an important role in the alleviation of inflammatory responses, the modulation of autophagy, apoptosis and ferroptosis, and the enhancement of anti-oxidative effect post-SCI. An increasing number of novel biomaterials have been fabricated as scaffolds and carriers, loaded with phytochemicals and drugs, to inhibit the progression of SCI through regulation of TLR4-NF-κB. This review summarizes the empirical strategies for the recovery after SCI through individual or composite biomaterials that mediate the TLR4-NF-κB signaling pathway.

摘要

脊髓损伤(SCI)后的修复和运动功能恢复仍然是一项临床挑战。损伤诱导的胶质增生和炎症会形成物理屏障以及极其抑制性的微环境,进而阻碍脊髓损伤的恢复。Toll样受体4(TLR4)-核因子κB(NF-κB)是一条经典的与植入物相关的固有免疫调节信号通路,也是众多基于生物材料的脊髓损伤治疗策略的一部分。大量实验研究表明,调节TLR4-NF-κB信号通路在减轻脊髓损伤后的炎症反应、调节自噬、凋亡和铁死亡以及增强抗氧化作用方面发挥着重要作用。越来越多的新型生物材料被制成支架和载体,负载植物化学物质和药物,以通过调节TLR4-NF-κB来抑制脊髓损伤的进展。本综述总结了通过介导TLR4-NF-κB信号通路的单一或复合生物材料促进脊髓损伤后恢复的经验策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2d1/9116428/bc817ee31d7e/fbioe-09-813169-g001.jpg

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