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本文引用的文献

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Macrophage and Fibroblast Interactions in Biomaterial-Mediated Fibrosis.生物材料介导的纤维化中的巨噬细胞和成纤维细胞相互作用。
Adv Healthc Mater. 2019 Feb;8(4):e1801451. doi: 10.1002/adhm.201801451. Epub 2019 Jan 18.
2
The M2a macrophage subset may be critically involved in the fibrogenesis of endometriosis in mice.M2a 巨噬细胞亚群可能在小鼠子宫内膜异位症的纤维化过程中起关键作用。
Reprod Biomed Online. 2018 Sep;37(3):254-268. doi: 10.1016/j.rbmo.2018.05.017. Epub 2018 Jun 30.
3
Functional muscle recovery with nanoparticle-directed M2 macrophage polarization in mice.纳米颗粒引导的 M2 巨噬细胞极化促进小鼠功能性肌肉恢复。
Proc Natl Acad Sci U S A. 2018 Oct 16;115(42):10648-10653. doi: 10.1073/pnas.1806908115. Epub 2018 Oct 1.
4
Controlled M1-to-M2 transition of aged macrophages by calcium phosphate coatings.通过磷酸钙涂层控制衰老巨噬细胞的 M1 到 M2 型转化。
Biomaterials. 2019 Mar;196:90-99. doi: 10.1016/j.biomaterials.2018.07.012. Epub 2018 Jul 17.
5
Dual release of growth factor from nanocomposite fibrous scaffold promotes vascularisation and bone regeneration in rat critical sized calvarial defect.纳米复合纤维支架双重释放生长因子促进大鼠临界尺寸颅骨缺损中的血管生成和骨再生。
Acta Biomater. 2018 Sep 15;78:36-47. doi: 10.1016/j.actbio.2018.07.050. Epub 2018 Jul 29.
6
PDGF-BB regulates splitting angiogenesis in skeletal muscle by limiting VEGF-induced endothelial proliferation.血小板衍生生长因子-BB 通过限制血管内皮生长因子诱导的内皮细胞增殖来调节骨骼肌肉中的血管生成。
Angiogenesis. 2018 Nov;21(4):883-900. doi: 10.1007/s10456-018-9634-5. Epub 2018 Jul 16.
7
Live imaging of wound angiogenesis reveals macrophage orchestrated vessel sprouting and regression.实时成像观察创伤血管生成揭示了巨噬细胞调控的血管出芽和退化。
EMBO J. 2018 Jul 2;37(13). doi: 10.15252/embj.201797786. Epub 2018 Jun 4.
8
The Role of Macrophages in Acute and Chronic Wound Healing and Interventions to Promote Pro-wound Healing Phenotypes.巨噬细胞在急性和慢性伤口愈合中的作用以及促进伤口愈合表型的干预措施。
Front Physiol. 2018 May 1;9:419. doi: 10.3389/fphys.2018.00419. eCollection 2018.
9
A Magnetically Responsive Biomaterial System for Flexibly Regulating the Duration between Pro- and Anti-Inflammatory Cytokine Deliveries.一种磁响应生物材料系统,用于灵活调节促炎细胞因子和抗炎细胞因子释放之间的时间间隔。
Adv Healthc Mater. 2018 Jun;7(12):e1800227. doi: 10.1002/adhm.201800227. Epub 2018 Apr 16.
10
3D-printed IFN-γ-loading calcium silicate-β-tricalcium phosphate scaffold sequentially activates M1 and M2 polarization of macrophages to promote vascularization of tissue engineering bone.3D 打印载 IFN-γ 的硅酸钙-β-三钙磷酸盐支架依次激活巨噬细胞 M1 和 M2 极化以促进组织工程骨血管化。
Acta Biomater. 2018 Apr 15;71:96-107. doi: 10.1016/j.actbio.2018.03.012. Epub 2018 Mar 14.

序贯药物递送调节巨噬细胞行为并增强植入物整合。

Sequential drug delivery to modulate macrophage behavior and enhance implant integration.

机构信息

Biomaterials and Regenerative Medicine Laboratory, School of Biomedical Engineering, Science, and Health Systems, Drexel University, Philadelphia, PA, United States.

Biomaterials and Regenerative Medicine Laboratory, School of Biomedical Engineering, Science, and Health Systems, Drexel University, Philadelphia, PA, United States.

出版信息

Adv Drug Deliv Rev. 2019 Sep-Oct;149-150:85-94. doi: 10.1016/j.addr.2019.05.005. Epub 2019 May 16.

DOI:10.1016/j.addr.2019.05.005
PMID:31103451
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6858522/
Abstract

Macrophages are major upstream regulators of the inflammatory response to implanted biomaterials. Sequential functions of distinct macrophage phenotypes are essential to the normal tissue repair process, which ideally results in vascularization and integration of implants. Improper timing of M1 or M2 macrophage activation results in dysfunctional healing in the form of chronic inflammation or fibrous encapsulation of the implant. Thus, biphasic drug delivery systems that modulate macrophage behavior are an appealing approach to promoting implant integration. In this review, we describe the timing and roles of macrophage phenotypes in healing, then highlight current drug delivery systems designed to sequentially modulate macrophage behavior.

摘要

巨噬细胞是植入生物材料引发炎症反应的主要上游调控者。不同表型的巨噬细胞的连续功能对于正常的组织修复过程至关重要,理想情况下会导致血管生成和植入物的整合。M1 或 M2 巨噬细胞激活时机不当会导致慢性炎症或植入物纤维包裹等功能失调的愈合。因此,调节巨噬细胞行为的两相药物传递系统是促进植入物整合的一种有吸引力的方法。在这篇综述中,我们描述了巨噬细胞表型在愈合过程中的时间和作用,然后重点介绍了目前设计用于连续调节巨噬细胞行为的药物传递系统。