研究动态
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椎间盘退变与炎症微环境:表达、病理及治疗策略。

Intervertebral disc degeneration and inflammatory microenvironment: expression, pathology, and therapeutic strategies.

发表日期:2023 Sep 04
作者: Xin Chen, Zihan Wang, Rongrong Deng, Hongjie Yan, Xin Liu, Ran Kang
来源: CYTOKINE & GROWTH FACTOR REVIEWS

摘要:

椎间盘退变(IDD)是腰背痛的主要原因之一,给社会经济带来重大负担。最近的研究突出了炎症微环境在IDD进展中的关键作用。我们在PubMed数据库中进行了基于关键词的搜索,寻找已发表的文章。炎症细胞因子的异常表达破坏了椎间盘(IVD)的稳态,导致它发生萎缩、纤维化和表型变化。调节炎症微环境和恢复细胞因子平衡有望实现IVD的修复与再生。本综述系统地考察了IDD中炎症微环境及相关细胞因子的表达调控、病理效应、治疗策略和未来挑战。关键的炎症细胞因子,包括白细胞介素(IL)、肿瘤坏死因子-α(TNF-α)和趋化因子,在IDD中表现出显著的病理效应。此外,化学拮抗剂、生物制剂、植物提取物和基因转录疗法等主要治疗模式被引入用于控制和改善炎症微环境。这些方法为未来IDD的抗炎治疗中的潜在靶点的鉴定提供了宝贵的见解。© 2023. 由于独家授权及 Springer Nature Switzerland AG。
Intervertebral disc degeneration (IDD) is a leading cause of low back pain (LBP), posing a significant socioeconomic burden. Recent studies highlight the crucial role of inflammatory microenvironment in IDD progression.A keyword-based search was performed using the PubMed database for published articles.Dysregulated expression of inflammatory cytokines disrupts intervertebral disc (IVD) homeostasis, causing atrophy, fibrosis, and phenotypic changes in nucleus pulposus cells. Modulating the inflammatory microenvironment and restoring cytokine balance hold promise for IVD repair and regeneration. This comprehensive review systematically examines the expression regulation, pathological effects, therapeutic strategies, and future challenges associated with the inflammatory microenvironment and relevant cytokines in IDD. Key inflammatory cytokines, including interleukins (IL), tumor necrosis factor-alpha (TNF-α), and chemokines, exhibit significant pathological effects in IDD. Furthermore, major therapeutic modalities such as chemical antagonists, biologics, plant extracts, and gene transcription therapies are introduced to control and ameliorate the inflammatory microenvironment. These approaches provide valuable insights for identifying potential targets in future anti-inflammatory treatments for IDD.© 2023. The Author(s), under exclusive licence to Springer Nature Switzerland AG.