An atlas of the aging lung mapped by single cell transcriptomics and deep tissue proteomics.

> 商业许可源文 · EUROPE_PMC · [CC-BY](https://creativecommons.org/licenses/by/)

书目信息

引用：Angelidis I, Simon LM, Fernandez IE, Strunz M, Mayr CH, Greiffo FR, Tsitsiridis G, Ansari M, Graf E, Strom TM, Nagendran M, Desai T, Eickelberg O, Mann M, Theis FJ, Schiller HB. (2019). An atlas of the aging lung mapped by single cell transcriptomics and deep tissue proteomics. Nature communications. PMID 30814501 · PMC6393476 · DOI 10.1038/s41467-019-08831-9

证据类型：DATABASE_RESOURCE

主题：rna-seq、single-cell、proteomics

被引次数（采集时）：538

原始记录：[Europe PMC](https://europepmc.org/article/MED/30814501)

来源许可：[CC-BY](https://creativecommons.org/licenses/by/)

作者摘要（按来源许可复用）

Aging promotes lung function decline and susceptibility to chronic lung diseases, which are the third leading cause of death worldwide. Here, we use single cell transcriptomics and mass spectrometry-based proteomics to quantify changes in cellular activity states across 30 cell types and chart the lung proteome of young and old mice. We show that aging leads to increased transcriptional noise, indicating deregulated epigenetic control. We observe cell type-specific effects of aging, uncovering increased cholesterol biosynthesis in type-2 pneumocytes and lipofibroblasts and altered relative frequency of airway epithelial cells as hallmarks of lung aging. Proteomic profiling reveals extracellular matrix remodeling in old mice, including increased collagen IV and XVI and decreased Fraser syndrome complex proteins and collagen XIV. Computational integration of the aging proteome with the single cell transcriptomes predicts the cellular source of regulated proteins and creates an unbiased reference map of the aging lung.

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