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在一种新的肺纤维化模型中鉴定纤维化间质性肺疾病病理生理学中的早期基因。

Identification of early genes in the pathophysiology of fibrotic interstitial lung disease in a new model of pulmonary fibrosis.

作者信息

Hennion Nathan, Bedart Corentin, Vandomber Léonie, Gottrand Frédéric, Humez Sarah, Chenivesse Cécile, Desseyn Jean-Luc, Gouyer Valérie

机构信息

Univ. Lille, Inserm, CHU Lille, Infinite U1286, Lille, F-59000, France.

Univ. Lille, Department of Pathology, CHU Lille, Lille, F-59000, France.

出版信息

Cell Mol Life Sci. 2025 Mar 13;82(1):115. doi: 10.1007/s00018-025-05620-0.

DOI:10.1007/s00018-025-05620-0
PMID:40074941
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11904048/
Abstract

Some interstitial lung diseases involve pulmonary fibrosis, which is a process that is characterized by the excessive and abnormal accumulation of extracellular matrix in the pulmonary interalveolar space. Although the current anti-fibrotic therapy aims at slowing down the progression of pulmonary fibrosis, it does not reverse it, and many of the drugs that were identified in basic-research studies failed in clinical phases, mainly because of the lack of a model that can recapitulate the pathophysiological mechanisms of human pulmonary fibrosis. We developed a novel experimental model of pulmonary fibrosis induced by a cocktail of molecules on an air/liquid interface culture of mouse embryonic lung explants. Histological analyses revealed a pattern of usual interstitial pneumonia, the worst-prognosis form of pulmonary fibrosis. We performed a transcriptomics analysis at the single-cell level after the induction of fibrosis and before any histological signs of fibrosis could be observed. The results revealed increased expression of several gene families that are involved in early inflammation, fibrosis and iron homeostasis, as well as potential new genetic targets.

摘要

一些间质性肺疾病会导致肺纤维化，这一过程的特征是细胞外基质在肺肺泡间隙过度且异常地积聚。尽管目前的抗纤维化疗法旨在减缓肺纤维化的进展，但无法使其逆转，而且许多在基础研究中发现的药物在临床阶段失败了，主要原因是缺乏一个能够重现人类肺纤维化病理生理机制的模型。我们在小鼠胚胎肺外植体的气/液界面培养中，利用一组分子开发了一种新型的肺纤维化实验模型。组织学分析显示出一种普通型间质性肺炎的模式，这是肺纤维化预后最差的形式。我们在诱导纤维化后且在观察到任何纤维化组织学迹象之前，在单细胞水平进行了转录组学分析。结果显示，参与早期炎症、纤维化和铁稳态的几个基因家族的表达增加，以及潜在的新基因靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa77/11904048/70f660583281/18_2025_5620_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa77/11904048/8520e7c8bd2e/18_2025_5620_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa77/11904048/f88ebcae0aa4/18_2025_5620_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa77/11904048/ab52a3597f9e/18_2025_5620_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa77/11904048/905b5fd43c9e/18_2025_5620_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa77/11904048/6103212f2bd0/18_2025_5620_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa77/11904048/1421f18926d9/18_2025_5620_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa77/11904048/19c7c3f9d64b/18_2025_5620_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa77/11904048/93c0922830d3/18_2025_5620_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa77/11904048/70f660583281/18_2025_5620_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa77/11904048/8520e7c8bd2e/18_2025_5620_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa77/11904048/f88ebcae0aa4/18_2025_5620_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa77/11904048/ab52a3597f9e/18_2025_5620_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa77/11904048/905b5fd43c9e/18_2025_5620_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa77/11904048/6103212f2bd0/18_2025_5620_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa77/11904048/1421f18926d9/18_2025_5620_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa77/11904048/19c7c3f9d64b/18_2025_5620_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa77/11904048/93c0922830d3/18_2025_5620_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa77/11904048/70f660583281/18_2025_5620_Fig9_HTML.jpg

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Progressive Pulmonary Fibrosis: Where Are We Now?进行性肺纤维化：我们目前的状况如何？
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