ArticleAmerican journal of respiratory cell and molecular biology2024
Transcriptomics Analysis Identifies the Decline in the Alveolar Type II Stem Cell Niche in Aged Human Lungs.
Article in American journal of respiratory cell and molecular biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 12 citations in OpenAlex.
- Fuelling repair: metabolic regulation of alveolar type 2 cell fate in lung regeneration and disease.Disease models & mechanisms · 2026Review
- The Gut-Lung Microbiome Axis in Alveolar Stem Cell Regeneration and Lung Repair.Microorganisms · 2026Review
- Cellular hallmarks and aging clock of the human lung parenchyma.Nature communications · 2026Article
- Spatial transcriptomics reveals compartment-specific cytotoxic T cell crosstalk with AT2 and goblet cells in advanced COPD.Biomarker research · 2026Article
- Epigenetic de-repression of basal cell metaplasia in aging AT2 cells is a risk factor for idiopathic pulmonary fibrosis (IPF).bioRxiv : the preprint server for biology · 2026Article
- Alveolar niche disruption and aberrant epithelial reprogramming are early hallmarks of idiopathic pulmonary fibrosis.bioRxiv : the preprint server for biology · 2026Article
- Syndecan-1 Promotes Alveolar Type 2 Epithelial Cell Senescence during Lung Fibrosis.bioRxiv : the preprint server for biology · 2026Article
- Article
- Single-cell atlas of human lung aging identifies cell type dyssynchrony and increased transcriptional entropy.Nature communications · 2026Article
- Cellular plasticity and regenerative mechanisms in the lung.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Aging-associated transcriptional programming of mitochondrial respiration in alveolar type II epithelial cells.Frontiers in cell and developmental biology · 2026Article
- Epithelial damage and ageing: the perfect storm.Thorax · 2025Review
- Alveolar epithelial cell plasticity and injury memory in human pulmonary fibrosis.bioRxiv : the preprint server for biology · 2025Article
- Aging directs the differential evolution of KRAS-driven lung adenocarcinoma.bioRxiv : the preprint server for biology · 2025Article
- Unveiling mechanisms of lung aging in COPD: A promising target for therapeutics development.Chinese medical journal pulmonary and critical care medicine · 2024Review
- Aging-Associated Molecular Changes in Human Alveolar Type I Cells.Journal of respiratory biology and translational medicine · 2024Article
- Lipids to the Rescue in Pulmonary Fibrosis: Biosynthesis, Bioenergetics, or Epigenetics?American journal of respiratory cell and molecular biology · 2024Article
- Arrestin beta 1 Regulates Alveolar Progenitor Renewal and Lung Fibrosis.Journal of respiratory biology and translational medicine · 2024Article
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6 authors at 2 institutions in 1 country.
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Abstract
Aging poses a global public health challenge, which is linked to the rise of age-related lung diseases. The precise understanding of the molecular and genetic changes in the aging lung that elevate the risk of acute and chronic lung diseases remains incomplete. Alveolar type II (AT2) cells are stem cells that maintain epithelial homeostasis and repair the lung after injury. AT2 progenitor function decreases with aging. The maintenance of AT2 function requires niche support from other cell types, but little has been done to characterize alveolar alterations with aging in the AT2 niche. To systematically profile the genetic changes associated with age, we present a single-cell transcriptional atlas comprising nearly half a million cells from the healthy lungs of human subjects spanning various ages, sexes, and smoking statuses. Most annotated cell lineages in aged lungs exhibit dysregulated genetic programs. Specifically, the aged AT2 cells demonstrate loss of epithelial identities, heightened inflammaging characterized by increased expression of AP-1 (Activator Protein-1) transcription factor and chemokine genes, and significantly increased cellular senescence. Furthermore, the aged mesenchymal cells display a remarkable decrease in collagen and elastin transcription and a loss of support to epithelial cell stemness. The decline of the AT2 niche is further exacerbated by a dysregulated genetic program in macrophages and dysregulated communications between AT2 and macrophages in aged human lungs. These findings highlight the dysregulations observed in both AT2 stem cells and their supportive niche cells, potentially contributing to the increased susceptibility of aged populations to lung diseases.
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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.