Insights gained in the pathology of lung disease through single‐cell transcriptomics
Insights gained in the pathology of lung disease through single‐cell transcriptomics
复制标题
通过单细胞转录组学获得肺部疾病病理学的见解
作者：
G. Carraro;B. Stripp
人的肺在正常健康状态下是一个相对静止的器官，但含有干细胞/祖细胞，有助于正常组织的维持，以及对损伤和疾病的修复或重塑。维护或修复导致功能肺组织的适当恢复和生理功能的维护，重塑导致结构和功能的改变，这通常与疾病有关。对参与肺组织维持和修复/重建的细胞类型的了解在很大程度上依赖于损伤修复和局部祖细胞的谱系追踪的小鼠模型。因此，人类肺部疾病重塑背后的许多功能改变仍未明确。然而，先进的基因组学方法在单细胞分辨率下定义肺细胞的分子表型的出现，为我们对正常人类肺内存在的细胞类型和伴随疾病的变化的理解铺平了道路。在这里，我们总结了从单细胞转录研究中出现的人类肺上皮分子表型与疾病相关变化的理解的最新进展。我们将注意力集中在上皮过渡状态的新兴概念上，这些概念表征了伴随着慢性肺部疾病的病理重塑，包括特发性肺纤维化、慢性阻塞性肺疾病、囊性纤维化和哮喘。这些研究产生的概念正在积极演变，需要进行确凿的研究来提高我们对疾病机制的理解。只要有可能，我们就强调在这一快速发展的研究领域提供统一命名的机会。©2022大不列颠和爱尔兰病理学会。
The human lung is a relatively quiescent organ in the normal healthy state but contains stem/progenitor cells that contribute to normal tissue maintenance and either repair or remodeling in response to injury and disease. Maintenance or repair lead to proper restoration of functional lung tissue and maintenance of physiological functions, with remodeling resulting in altered structure and function that is typically associated with disease. Knowledge of cell types contributing to lung tissue maintenance and repair/remodeling have largely relied on mouse models of injury‐repair and lineage tracing of local progenitors. Therefore, many of the functional alterations underlying remodeling in human lung disease have remained poorly defined. However, the advent of advanced genomics approaches to define the molecular phenotype of lung cells at single‐cell resolution has paved the way for rapid advances in our understanding of cell types present within the normal human lung and changes that accompany disease. Here we summarize recent advances in our understanding of disease‐related changes in the molecular phenotype of human lung epithelium that have emerged from single‐cell transcriptomic studies. We focus attention on emerging concepts of epithelial transitional states that characterize the pathological remodeling that accompanies chronic lung diseases, including idiopathic pulmonary fibrosis, chronic obstructive pulmonary disease, cystic fibrosis, and asthma. Concepts arising from these studies are actively evolving and require corroborative studies to improve our understanding of disease mechanisms. Whenever possible, we highlight opportunities for providing a unified nomenclature in this rapidly advancing field of research. © 2022 The Pathological Society of Great Britain and Ireland.
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DOI：
10.1164/rccm.201808-1543oc
发表时间：
2019-05
影响因子：
24.7
作者：
Wei Wu;Seo-Jin Bang;E. Bleecker;M. Castro;L. Denlinger;S. Erzurum;J. Fahy;A. Fitzpatrick;B. Gaston;A. Hastie;E. Israel;N. Jarjour;B. Levy;D. Mauger;D. Meyers;W. Moore;M. Peters;B. Phillips;W. Phipatanakul;R. Sorkness;S. Wenzel
通讯作者：
Wei Wu;Seo-Jin Bang;E. Bleecker;M. Castro;L. Denlinger;S. Erzurum;J. Fahy;A. Fitzpatrick;B. Gaston;A. Hastie;E. Israel;N. Jarjour;B. Levy;D. Mauger;D. Meyers;W. Moore;M. Peters;B. Phillips;W. Phipatanakul;R. Sorkness;S. Wenzel
影响因子：
6.4
作者：
R. Tuder;I. Petrache;J. Elias;N. Voelkel;P. Henson
通讯作者：
R. Tuder;I. Petrache;J. Elias;N. Voelkel;P. Henson
影响因子：
9.6
作者：
Miller, Marina;Cho, Jae Youn;Broide, David H.
通讯作者：
Broide, David H.
影响因子：
5
作者：
Baumgartner, KB;Samet, JM;Waldron, JA
通讯作者：
Waldron, JA
DOI：
10.1513/pats.200605-105sf
发表时间：
2006-11-01
期刊：
Proceedings of the American Thoracic Society
影响因子：
--
作者：
Taraseviciene-Stewart, Laima;Douglas, Ivor S;Voelkel, Norbert F
通讯作者：
Voelkel, Norbert F