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Emerging insights in sarcoidosis: moving forward through reverse translational research.结节病研究新进展:通过反向转化医学研究不断前进。
Am J Physiol Lung Cell Mol Physiol. 2022 Apr 1;322(4):L518-L525. doi: 10.1152/ajplung.00266.2021. Epub 2022 Feb 23.
2
Molecular Mechanism in the Development of Pulmonary Fibrosis in Patients with Sarcoidosis.结节病患者肺纤维化发展中的分子机制。
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From granuloma to fibrosis: sarcoidosis associated pulmonary fibrosis.从肉芽肿到纤维化:结节病相关的肺纤维化。
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Elevated IL-15 concentrations in the sarcoidosis lung are independent of granuloma burden and disease phenotypes.结节病肺部的白细胞介素-15 浓度升高与肉芽肿负担和疾病表型无关。
Am J Physiol Lung Cell Mol Physiol. 2021 Jun 1;320(6):L1137-L1146. doi: 10.1152/ajplung.00575.2020. Epub 2021 Apr 14.
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ApoE-deficient mice on cholate-containing high-fat diet reveal a pathology similar to lung sarcoidosis.载脂蛋白 E 缺陷型小鼠在含鹅脱氧胆酸的高脂肪饮食下可出现类似结节病的肺部病理学改变。
Am J Pathol. 2010 Mar;176(3):1148-56. doi: 10.2353/ajpath.2010.090857. Epub 2010 Jan 21.
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Circulating cytokines in sarcoidosis: phenotype-specific alterations for fibrotic and non-fibrotic pulmonary disease.结节病中的循环细胞因子:纤维化和非纤维化肺部疾病的表型特异性改变。
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Novel insights in fibrotic pulmonary sarcoidosis.纤维化性肺结节病的新见解。
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Animal models of sarcoidosis.结节病的动物模型。
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The clinical and immunologic features of pulmonary fibrosis in sarcoidosis.结节病性肺纤维化的临床和免疫学特征。
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Plasma collagen neoepitopes are associated with multiorgan disease in the ACCESS and GRADS sarcoidosis cohorts.血浆胶原新表位与 ACCESS 和 GRADS 结节病队列中的多器官疾病相关。
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Circulating Mitochondrial DNA Is Associated With High Levels of Fatigue in Two Independent Sarcoidosis Cohorts.循环线粒体 DNA 与两个独立的结节病队列中的高疲劳水平相关。
Chest. 2024 May;165(5):1174-1185. doi: 10.1016/j.chest.2023.11.020. Epub 2023 Nov 15.
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Is this the Dawning of AI for Sarcoidosis?这是结节病人工智能时代的曙光吗?
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From Karl Wurm and Guy Scadding's staging to F-FDG PET/CT scan phenotyping and far beyond: perspective in the evading history of phenotyping in sarcoidosis.从卡尔·武尔姆和盖伊·斯卡丁的分期到氟代脱氧葡萄糖正电子发射断层显像/计算机断层扫描(F-FDG PET/CT)扫描表型分析,乃至更广泛的领域:结节病表型分析的曲折历史透视
Front Med (Lausanne). 2023 May 10;10:1174518. doi: 10.3389/fmed.2023.1174518. eCollection 2023.

本文引用的文献

1
Roles of Macrophage Polarization and Macrophage-Derived miRNAs in Pulmonary Fibrosis.巨噬细胞极化及巨噬细胞衍生 miRNA 在肺纤维化中的作用。
Front Immunol. 2021 Aug 13;12:678457. doi: 10.3389/fimmu.2021.678457. eCollection 2021.
2
Transcriptomics of bronchoalveolar lavage cells identifies new molecular endotypes of sarcoidosis.支气管肺泡灌洗细胞的转录组学鉴定了结节病的新分子内型。
Eur Respir J. 2021 Dec 2;58(6). doi: 10.1183/13993003.02950-2020. Print 2021 Dec.
3
Elevated IL-15 concentrations in the sarcoidosis lung are independent of granuloma burden and disease phenotypes.结节病肺部的白细胞介素-15 浓度升高与肉芽肿负担和疾病表型无关。
Am J Physiol Lung Cell Mol Physiol. 2021 Jun 1;320(6):L1137-L1146. doi: 10.1152/ajplung.00575.2020. Epub 2021 Apr 14.
4
Novel three-dimensional biochip pulmonary sarcoidosis model.新型三维生物芯片肺结节病模型。
PLoS One. 2021 Feb 4;16(2):e0245805. doi: 10.1371/journal.pone.0245805. eCollection 2021.
5
Single Cell Transcriptomics Implicate Novel Monocyte and T Cell Immune Dysregulation in Sarcoidosis.单细胞转录组学提示新型单核细胞和 T 细胞免疫失调与结节病有关。
Front Immunol. 2020 Dec 8;11:567342. doi: 10.3389/fimmu.2020.567342. eCollection 2020.
6
Translational Research in the Time of COVID-19-Dissolving Boundaries.新冠疫情时代的转化研究——消除界限
PLoS Pathog. 2020 Sep 30;16(9):e1008898. doi: 10.1371/journal.ppat.1008898. eCollection 2020 Sep.
7
Phagosome-regulated mTOR signalling during sarcoidosis granuloma biogenesis.吞噬体调节的肌醇三磷酸信号通路在肉样瘤肉芽肿发生中的作用。
Eur Respir J. 2021 Mar 18;57(3). doi: 10.1183/13993003.02695-2020. Print 2021 Mar.
8
Schisandra Inhibit Bleomycin-Induced Idiopathic Pulmonary Fibrosis in Rats via Suppressing M2 Macrophage Polarization.五味子通过抑制 M2 型巨噬细胞极化抑制博来霉素诱导的大鼠特发性肺纤维化。
Biomed Res Int. 2020 Aug 20;2020:5137349. doi: 10.1155/2020/5137349. eCollection 2020.
9
Current Sarcoidosis Models and the Importance of Focusing on the Granuloma.当前的肉样瘤病模型和关注肉芽肿的重要性。
Front Immunol. 2020 Aug 4;11:1719. doi: 10.3389/fimmu.2020.01719. eCollection 2020.
10
Novel protein pathways in development and progression of pulmonary sarcoidosis.肺结节病发生发展中的新蛋白通路。
Sci Rep. 2020 Aug 6;10(1):13282. doi: 10.1038/s41598-020-69281-8.

结节病研究新进展:通过反向转化医学研究不断前进。

Emerging insights in sarcoidosis: moving forward through reverse translational research.

机构信息

Section of Pulmonary, Critical Care, and Sleep Medicine, Yale School of Medicine, Yale University, New Haven, Connecticut.

出版信息

Am J Physiol Lung Cell Mol Physiol. 2022 Apr 1;322(4):L518-L525. doi: 10.1152/ajplung.00266.2021. Epub 2022 Feb 23.

DOI:10.1152/ajplung.00266.2021
PMID:35196896
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8957321/
Abstract

Sarcoidosis is a chronic granulomatous disease of unknown etiology that primarily affects the lungs. The development of stage IV or fibrotic lung disease accounts for a significant proportion of the morbidity and mortality attributable to sarcoidosis. Further investigation into the active mechanisms of disease pathogenesis and fibrogenesis might illuminate fundamental mediators of injury and repair while providing new opportunities for clinical intervention. However, progress in sarcoidosis research has been hampered by the heterogeneity of clinical phenotypes and the lack of a consensus modeling system. Recently, reverse translational research, wherein observations made at the patient level catalyze hypothesis-driven research at the laboratory bench, has generated new discoveries regarding the immunopathogenic mechanisms of pulmonary granuloma formation, fibrogenesis, and disease model development. The purpose of this review is to highlight the promise and possibility of these novel investigative efforts.

摘要

结节病是一种病因不明的慢性肉芽肿性疾病,主要影响肺部。第四阶段或纤维化肺病的发展是结节病发病率和死亡率的重要原因。进一步研究疾病发病机制和纤维化形成的活跃机制可以阐明损伤和修复的基本介质,同时为临床干预提供新的机会。然而,结节病研究的进展受到临床表型的异质性和缺乏共识建模系统的阻碍。最近,反向转化研究,即患者层面的观察结果促进实验室研究的假设驱动研究,已经发现了关于肺肉芽肿形成、纤维化和疾病模型发展的免疫发病机制的新发现。本文的目的是强调这些新的研究努力的潜力和可能性。