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本文引用的文献

1
Accumulation of cholesterol suppresses oxidative phosphorylation and altered responses to inflammatory stimuli of macrophages.胆固醇的积累会抑制氧化磷酸化,并改变巨噬细胞对炎症刺激的反应。
Biochem Biophys Rep. 2021 Nov 3;28:101166. doi: 10.1016/j.bbrep.2021.101166. eCollection 2021 Dec.
2
Therapeutic Effects of Azithromycin on Spinal Cord Injury in Male Wistar Rats: A Role for Inflammatory Pathways.阿奇霉素对雄性 Wistar 大鼠脊髓损伤的治疗作用:炎症通路的作用。
J Neurol Surg A Cent Eur Neurosurg. 2022 Sep;83(5):411-419. doi: 10.1055/s-0041-1735854. Epub 2021 Nov 15.
3
The role of miR-27b-3p/HOXA10 axis in the pathogenesis of endometriosis.miR-27b-3p/HOXA10轴在子宫内膜异位症发病机制中的作用。
Ann Palliat Med. 2021 Mar;10(3):3162-3170. doi: 10.21037/apm-21-343.
4
Macrophage-derived netrin-1 contributes to endometriosis-associated pain.巨噬细胞衍生的netrin-1导致子宫内膜异位症相关疼痛。
Ann Transl Med. 2021 Jan;9(1):29. doi: 10.21037/atm-20-2161.
5
Top 10 priorities for future infertility research: an international consensus development study†  ‡.未来不孕不育研究的 10 大重点:国际共识发展研究†‡。
Hum Reprod. 2020 Dec 1;35(12):2715-2724. doi: 10.1093/humrep/deaa242.
6
Use of Cannabis for Self-Management of Chronic Pelvic Pain.大麻在慢性盆腔痛自我管理中的应用。
J Womens Health (Larchmt). 2021 Sep;30(9):1344-1351. doi: 10.1089/jwh.2020.8737. Epub 2020 Nov 16.
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The Endometrioma Treatment Paradigm when Fertility Is Desired: A Systematic Review.当期望生育时的子宫内膜异位症治疗模式:系统评价。
J Minim Invasive Gynecol. 2021 Mar;28(3):575-586. doi: 10.1016/j.jmig.2020.11.020. Epub 2020 Nov 26.
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Deficiency of Inositol Monophosphatase Activity Decreases Phosphoinositide Lipids and Enhances TRPV1 Function .肌醇单磷酸酶活性缺乏降低磷酸肌醇脂质并增强 TRPV1 功能。
J Neurosci. 2021 Jan 20;41(3):408-423. doi: 10.1523/JNEUROSCI.0803-20.2020. Epub 2020 Nov 25.
9
Relationship between the severity of endometriosis symptoms (dyspareunia, dysmenorrhea and chronic pelvic pain) and the spread of the disease on ultrasound.子宫内膜异位症症状(性交疼痛、痛经和慢性盆腔疼痛)的严重程度与超声检查下疾病扩散情况之间的关系。
BMC Res Notes. 2020 Nov 25;13(1):546. doi: 10.1186/s13104-020-05388-5.
10
Pain in Endometriosis.子宫内膜异位症中的疼痛
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炎症介导的巨噬细胞极化在内异症中诱导TRPV1/TRPA1异聚体形成。

Inflammation-mediated macrophage polarization induces TRPV1/TRPA1 heteromers in endometriosis.

作者信息

Zhu Hai, Wang Yi, He Yibo, Yu Weifeng

机构信息

Department of Anesthesiology, Second Military Medical University Affiliated Eastern Hepatobiliary Surgery Hospital 255 Changhai Road, Yangpu District, Shanghai, China.

Department of Anesthesiology, Shanghai Putuo Maternity and Infant Health Hospital 517 Tongpu Road, Putuo District, Shanghai, China.

出版信息

Am J Transl Res. 2022 May 15;14(5):3066-3078. eCollection 2022.

PMID:35702089
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9185066/
Abstract

Chronic pelvic pain (CPP) and infertility are the common characteristics of endometriosis. Macrophages and related inflammation play important roles in endometriosis pain. TRPV1 and TRPA1 form a heteromeric channel which is related to endometriosis pain. In the present study, the inflammation-mediated macrophage polarization along with TRPV1/TRPA1 heteromers in endometriosis was investigated and . Macrophage polarization and TRPV1/TRPA1 heteromers in endometriosis tissue of patients were assayed, and was further investigated in endometriosis mice by co-culturing macrophages derived from mice in different groups with human endometrium cells. Our results indicated that macrophage polarization, as CD86 and CD206 positive macrophages, were accompanied by TRPV1/TRPA1 heteromers in endometriosis tissues of patients with pain. Inflammatory factors in peritoneal lavage fluid and serum of mice were correlated with TRPV1/TRPA1 expression in endometriosis tissues of mice as well as macrophage polarization which tended to be consistent with TRPV1/TRPA1 heteromers in endometriosis tissue. Moreover, macrophage polarization in enterocoelia induced ectopic endometrial cells migration with the increase in TRPV1/TRPA1 heteromers. Our results suggest that endometriosis-induced celiac inflammation might mediate macrophage polarization along with the increase of TRPV1/TRPA1 heteromers, which may play a key role in endometriosis pain.

摘要

慢性盆腔疼痛(CPP)和不孕是子宫内膜异位症的常见特征。巨噬细胞及相关炎症在子宫内膜异位症疼痛中起重要作用。TRPV1和TRPA1形成一种与子宫内膜异位症疼痛相关的异源通道。在本研究中,对炎症介导的巨噬细胞极化以及子宫内膜异位症中TRPV1/TRPA1异聚体进行了研究。检测了患者子宫内膜异位症组织中的巨噬细胞极化和TRPV1/TRPA1异聚体,并通过将不同组小鼠来源的巨噬细胞与人子宫内膜细胞共培养,在子宫内膜异位症小鼠中进一步研究。我们的结果表明,在有疼痛的患者子宫内膜异位症组织中,作为CD86和CD206阳性巨噬细胞的巨噬细胞极化与TRPV1/TRPA1异聚体同时存在。小鼠腹腔灌洗液和血清中的炎症因子与小鼠子宫内膜异位症组织中TRPV1/TRPA1的表达以及巨噬细胞极化相关,而巨噬细胞极化倾向于与子宫内膜异位症组织中的TRPV1/TRPA1异聚体一致。此外,腹腔内巨噬细胞极化随着TRPV1/TRPA1异聚体的增加诱导异位子宫内膜细胞迁移。我们的结果表明,子宫内膜异位症诱导的腹腔炎症可能介导巨噬细胞极化以及TRPV1/TRPA1异聚体的增加,这可能在子宫内膜异位症疼痛中起关键作用。