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肺纤维化中的细胞间相互作用与通讯动态

Cell-cell interactions and communication dynamics in lung fibrosis.

作者信息

Xie Ting, Liang Jiurong, Stripp Barry, Noble Paul W

机构信息

Division of Pulmonary and Critical Care Medicine, Department of Medicine, Women's Guild Lung Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.

出版信息

Chin Med J Pulm Crit Care Med. 2024 Jun 18;2(2):63-71. doi: 10.1016/j.pccm.2024.04.001. eCollection 2024 Jun.

DOI:10.1016/j.pccm.2024.04.001
PMID:39169931
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11332853/
Abstract

Cell-cell interactions are essential components of coordinated cell function in lung homeostasis. Lung diseases involve altered cell-cell interactions and communication between different cell types, as well as between subsets of cells of the same type. The identification and understanding of intercellular signaling in lung fibrosis offer insights into the molecular mechanisms underlying these interactions and their implications in the development and progression of lung fibrosis. A comprehensive cell atlas of the human lung, established with the facilitation of single-cell RNA transcriptomic analysis, has enabled the inference of intercellular communications using ligand-receptor databases. In this review, we provide a comprehensive overview of the modified cell-cell communications in lung fibrosis. We highlight the intricate interactions among the major cell types within the lung and their contributions to fibrogenesis. The insights presented in this review will contribute to a better understanding of the molecular mechanisms underlying lung fibrosis and may guide future research efforts in developing targeted therapies for this debilitating disease.

摘要

细胞间相互作用是肺内稳态中细胞协调功能的重要组成部分。肺部疾病涉及不同细胞类型之间以及同一类型细胞亚群之间细胞间相互作用和通讯的改变。肺纤维化中细胞间信号传导的识别与理解为这些相互作用的分子机制及其在肺纤维化发生发展中的意义提供了见解。借助单细胞RNA转录组分析建立的人类肺脏综合细胞图谱,使得利用配体-受体数据库推断细胞间通讯成为可能。在本综述中,我们全面概述了肺纤维化中细胞间通讯的改变。我们强调了肺内主要细胞类型之间复杂的相互作用及其对纤维化形成的作用。本综述所呈现的见解将有助于更好地理解肺纤维化的分子机制,并可能为开发针对这种使人衰弱疾病的靶向治疗方法的未来研究工作提供指导。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7730/11332853/11d873c30933/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7730/11332853/21b8b4a92dd2/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7730/11332853/11d873c30933/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7730/11332853/21b8b4a92dd2/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7730/11332853/11d873c30933/gr2.jpg

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Nat Commun. 2023 Aug 31;14(1):4956. doi: 10.1038/s41467-023-40617-y.
2
The lung mesenchyme in development, regeneration, and fibrosis.发育、再生和纤维化中的肺间质。
J Clin Invest. 2023 Jul 17;133(14):e170498. doi: 10.1172/JCI170498.
3
Senescence of alveolar epithelial progenitor cells: a critical driver of lung fibrosis.肺泡上皮祖细胞衰老:肺纤维化的关键驱动因素。
Am J Physiol Cell Physiol. 2023 Aug 1;325(2):C483-C495. doi: 10.1152/ajpcell.00239.2023. Epub 2023 Jul 17.
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Reciprocal interactions between alveolar progenitor dysfunction and aging promote lung fibrosis.肺泡祖细胞功能障碍和衰老之间的相互作用促进肺纤维化。
Elife. 2023 Jun 14;12:e85415. doi: 10.7554/eLife.85415.
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An integrated cell atlas of the lung in health and disease.肺部健康与疾病的细胞整合图谱
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Maladaptive TGF-β Signals to the Alveolar Epithelium Drive Fibrosis after COVID-19 Infection.新冠病毒感染后,向肺泡上皮细胞发出的适应性不良转化生长因子-β信号驱动纤维化。
Am J Respir Crit Care Med. 2023 Jul 15;208(2):201-204. doi: 10.1164/rccm.202302-0264LE.
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Nat Commun. 2023 Apr 28;14(1):2445. doi: 10.1038/s41467-023-38134-z.
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