ArticleNature communications2019
An atlas of the aging lung mapped by single cell transcriptomics and deep tissue proteomics.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 394 papers, 4 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
394 citing papers in PubMed, 4 syntheses or guidelines pooled it, 655 citations in OpenAlex.
- Shared and niche-specific transcriptional signatures of macrophage aging revealed by a cross-tissue meta-analysis.BMC biology · 2026Pooled it
- Advances in Molecular Research of Tracheobronchial Tree Aging: A Systematic Review.International journal of molecular sciences · 2025Pooled it
- Peripheral blood monocyte count and outcomes in patients with interstitial lung disease: a systematic review and meta-analysis.European respiratory review : an official journal of the European Respiratory Society · 2023Pooled it
- Genome-wide association study of lung adenocarcinoma in East Asia and comparison with a European population.Nature communications · 2023Pooled it
- RamanOmics decodes the spatial vibrational-molecular architecture of senescence in aging and repair.Nature aging · 2026Article
- Lineage identity governs oncogene dependence in mouse NSCLC models of KRAS inhibitor resistance.Nature genetics · 2026Article
- Restoring the FOXO1 geroprotective pathway via seno-resistant mesenchymal progenitor cells alleviates primate epididymal aging.Protein & cell · 2026Article
- DEAPLOG: Differential Expression Analysis and Pseudo-Temporal Locating and Ordering of Genes in Single-Cell Transcriptomic Data.Interdisciplinary sciences, computational life sciences · 2026Article
- NAMPT activation uncovers a senescence-specific vulnerability and promotes healthy aging in combination with NAM.bioRxiv : the preprint server for biology · 2026Article
- [Misdirected intercellular communication in aging and chronic inflammation].Zeitschrift fur Gerontologie und Geriatrie · 2026Review
- An immune-poised state of human bronchial epithelial cells mediates defense against RSV in adults.Nature communications · 2026Article
- Cellular hallmarks and aging clock of the human lung parenchyma.Nature communications · 2026Article
- Assessing Transduction Efficiency And Cell Targeting By Cell-penetrating Peptides In The Mouse Lung.Journal of visualized experiments : JoVE · 2026Article
- Oncogenic KRAS-driven type I interferon signalling primes pancreatic cancer for necroptosis.Nature communications · 2026Article
- Single-nucleus interrogation of primate small intestinal aging reveals NCoR1 decline as a conserved feature that is reversed by metformin.Nature aging · 2026Article
- High altitude-mediated immune remodeling accelerates aging.Science advances · 2026Article
- Pollutant particles enhance house dust mite induced type 2 inflammation and the recruitment of monocyte derived Cd11cParticle and fibre toxicology · 2026Article
- Article
- Gene expression and co-expression heterogeneity patterns and biodemography analyses during the cell cycle encourage aging studies in archaea.GeroScience · 2026Article
- CellVoyager: AI CompBio agent generates new insights by autonomously analyzing biological data.Nature methods · 2026Article
334 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.