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本文引用的文献

1
Revisiting estrogen-dependent signaling pathways in endometriosis: Potential targets for non-hormonal therapeutics.重新审视子宫内膜异位症中雌激素依赖性信号通路:非激素治疗的潜在靶点。
Eur J Obstet Gynecol Reprod Biol. 2021 Mar;258:103-110. doi: 10.1016/j.ejogrb.2020.12.044. Epub 2020 Dec 29.
2
The miR-23a∼27a∼24-2 microRNA Cluster Promotes Inflammatory Polarization of Macrophages.miR-23a∼27a∼24-2 微 RNA 簇促进巨噬细胞的炎症极化。
J Immunol. 2021 Feb 1;206(3):540-553. doi: 10.4049/jimmunol.1901277. Epub 2020 Dec 16.
3
In vitro and in vivo evaluation of anti-tumoral effect of M1 phenotype induction in macrophages by miR-130 and miR-33 containing exosomes.通过 miR-130 和 miR-33 载带的外泌体诱导巨噬细胞中 M1 表型的体内外抗肿瘤效果评估。
Cancer Immunol Immunother. 2021 May;70(5):1323-1339. doi: 10.1007/s00262-020-02762-x. Epub 2020 Nov 3.
4
Activation of M1 Macrophages in Response to Recombinant TB Vaccines With Enhanced Antimycobacterial Activity.针对具有增强抗分枝杆菌活性的重组结核疫苗,M1 巨噬细胞的激活。
Front Immunol. 2020 Jun 23;11:1298. doi: 10.3389/fimmu.2020.01298. eCollection 2020.
5
Macrophage Modification Strategies for Efficient Cell Therapy.巨噬细胞修饰策略用于高效细胞治疗。
Cells. 2020 Jun 24;9(6):1535. doi: 10.3390/cells9061535.
6
Endometriosis Patients Show an Increased M2 Response in the Peritoneal CD14/CD68 Macrophage Subpopulation Coupled with an Increase in the T-helper 2 and T-regulatory Cells.子宫内膜异位症患者的腹腔 CD14/CD68 巨噬细胞亚群中 M2 反应增加,同时辅助性 T 细胞 2 和调节性 T 细胞增加。
Reprod Sci. 2020 Oct;27(10):1920-1931. doi: 10.1007/s43032-020-00211-9. Epub 2020 Jun 22.
7
Tumor-Associated Macrophages: Recent Insights and Therapies.肿瘤相关巨噬细胞:最新见解与治疗方法
Front Oncol. 2020 Feb 25;10:188. doi: 10.3389/fonc.2020.00188. eCollection 2020.
8
Autonomic nervous system and inflammation interaction in endometriosis-associated pain.子宫内膜异位症相关疼痛中的自主神经系统与炎症的相互作用。
J Neuroinflammation. 2020 Mar 7;17(1):80. doi: 10.1186/s12974-020-01752-1.
9
IL-17A Modulates Peritoneal Macrophage Recruitment and M2 Polarization in Endometriosis.白细胞介素-17A调节子宫内膜异位症中腹膜巨噬细胞的募集和M2极化。
Front Immunol. 2020 Feb 14;11:108. doi: 10.3389/fimmu.2020.00108. eCollection 2020.
10
Regulation of Inflammation Pathways and Inflammasome by Sex Steroid Hormones in Endometriosis.子宫内膜异位症中甾体性激素对炎症信号通路和炎性小体的调控
Front Endocrinol (Lausanne). 2020 Jan 29;10:935. doi: 10.3389/fendo.2019.00935. eCollection 2019.

子宫内膜异位症与癌症:巨噬细胞作用的探索。

Endometriosis and Cancer: Exploring the Role of Macrophages.

机构信息

Scientific Research Institute of Human Morphology, 117418 Moscow, Russia.

National Medical Research Center for Obstetrics, Gynecology and Perinatology Named after Academician V.I., Kulakov of Ministry of Healthcare of Russian Federation, 117997 Moscow, Russia.

出版信息

Int J Mol Sci. 2021 May 14;22(10):5196. doi: 10.3390/ijms22105196.

DOI:10.3390/ijms22105196
PMID:34068967
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8156385/
Abstract

Endometriosis and cancer have much in common, notably their burgeoning of cells in hypoxic milieus, their invasiveness, and their capacity to trigger remodeling, vascularization, and innervation of other tissues. An important role in these processes is played by permissive microenvironments inhabited by a variety of stromal and immune cells, including macrophages. Remarkable phenotypical plasticity of macrophages makes them a promising therapeutic target; some key issues are the range of macrophage phenotypes characteristic of a particular pathology and the possible manners of its modulation. In both endometriosis and cancer, macrophages guard the lesions from immune surveillance while promoting pathological cell growth, invasion, and metastasis. This review article focuses on a comparative analysis of macrophage behaviors in endometriosis and cancer. We also highlight recent reports on the experimental modulation of macrophage phenotypes in preclinical models of endometriosis and cancer.

摘要

子宫内膜异位症和癌症有许多共同之处,特别是它们在缺氧环境中细胞的过度生长、侵袭性以及触发其他组织重塑、血管生成和神经支配的能力。各种基质细胞和免疫细胞(包括巨噬细胞)居住的有利微环境在这些过程中起着重要作用。巨噬细胞显著的表型可塑性使它们成为有前途的治疗靶点;一些关键问题是特定病理学特征的巨噬细胞表型范围及其可能的调节方式。在子宫内膜异位症和癌症中,巨噬细胞保护病变免受免疫监视,同时促进病理性细胞生长、侵袭和转移。本文重点对子宫内膜异位症和癌症中巨噬细胞行为进行比较分析。我们还强调了最近关于在子宫内膜异位症和癌症的临床前模型中实验调节巨噬细胞表型的报告。