巨噬细胞在种植体磨损碎片诱导的假体周围骨溶解中的全身运输。

IF 2.5 4区医学 Q3 BIOCHEMICAL RESEARCH METHODS

SLAS Technology Pub Date : 2025-02-04 DOI:10.1016/j.slast.2025.100254

Mengyun Lou

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引用次数: 0

摘要

假体周围骨溶解（PPOL）是关节置换术后的一个重要并发症，通常由假体磨损碎片引起，导致慢性炎症和骨吸收。本文综述了PPOL的免疫机制，特别是巨噬细胞被植入物磨损碎片招募的过程，巨噬细胞触发炎症级联反应的机制，以及促进巨噬细胞迁移的趋化因子的作用，包括CCL2、CCL3、CCL4、CCL5、CXCL8、CX3CL1和XCL1。这篇综述强调了这些过程的新发现，并表明阐明这些机制为未来预防和治疗PPOL的治疗策略提供了有希望的途径，例如抗炎药物的潜在使用。

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Systemic trafficking of macrophages in implant wear debris-induced periprosthetic osteolysis

Periprosthetic osteolysis (PPOL) is a significant complication post-joint replacement, often instigated by implant wear debris, leading to chronic inflammation and bone resorption. Herein, this review summarizes the immune mechanisms of PPOL, specifically, the processes where macrophages are recruited by implant wear debris, the mechanisms by which macrophages trigger inflammatory cascades, and the role of chemokines that facilitate macrophage migration, including CCL2, CCL3, CCL4, CCL5, CXCL8, CX3CL1, and XCL1. This review highlights novel findings on these processes and suggests that illustrating these mechanisms offers promising avenues for future therapeutic strategies to prevent and treat PPOL, such as the potential use of anti-inflammatory drugs.

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来源期刊

SLAS Technology Computer Science-Computer Science Applications

CiteScore

6.30

自引率

7.40%

发文量

审稿时长

106 days

期刊介绍： SLAS Technology emphasizes scientific and technical advances that enable and improve life sciences research and development; drug-delivery; diagnostics; biomedical and molecular imaging; and personalized and precision medicine. This includes high-throughput and other laboratory automation technologies; micro/nanotechnologies; analytical, separation and quantitative techniques; synthetic chemistry and biology; informatics (data analysis, statistics, bio, genomic and chemoinformatics); and more.