ArticleNature communications2022
Consequences of telomere dysfunction in fibroblasts, club and basal cells for lung fibrosis development.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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
19 citing papers in PubMed, 30 citations in OpenAlex.
- Age-dependent mitochondrial toxicity in renal stem cells: A precise 3D silk matrix model.Genes & diseases · 2026Article
- Spatial Distribution of K13-Positive Airway Epithelial Cells in Idiopathic Pulmonary Fibrosis.Biomedicines · 2026Article
- Aging and lung diseases: Unraveling mechanisms and therapeutic targets.Chinese medical journal pulmonary and critical care medicine · 2025Review
- Telomere Dysfunction in Renal Tubular Epithelial Cells Leads to Kidney Fibrosis.Journal of the American Society of Nephrology : JASN · 2025Article
- Telomerase modRNA Offers a Novel RNA-Based Approach to Treat Human Pulmonary Fibrosis.Aging cell · 2025Article
- Article
- Gender-based differences in telomere attrition and long-term respiratory dysfunction in COVID-19 ICU survivors one year post-infection: implications for aging-associated pulmonary decline.Frontiers in immunology · 2025Article
- Regenerative Capacity of Alveolar Type 2 Cells Is Proportionally Reduced Following Disease Progression in Idiopathic Pulmonary Fibrosis-Derived Organoid Cultures.Tuberculosis and respiratory diseases · 2025Article
- Renal fibroblasts are involved in fibrogenic changes in kidney fibrosis associated with dysfunctional telomeres.Experimental & molecular medicine · 2024Article
- Genetics and Genomics of Pulmonary Fibrosis: Charting the Molecular Landscape and Shaping Precision Medicine.American journal of respiratory and critical care medicine · 2024Review
- Differential contribution for ERK1 and ERK2 kinases in BRAFCell death and differentiation · 2024Article
- Article
- Different Role of TRF1 and TRF2 Expression in Non-Small Cell Lung Cancers.OncoTargets and therapy · 2024Article
- A new variant in theERJ open research · 2024Article
- Short airway telomeres are associated with primary graft dysfunction and chronic lung allograft dysfunction.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2023Article
- Senescence of alveolar epithelial progenitor cells: a critical driver of lung fibrosis.American journal of physiology. Cell physiology · 2023Review
- Article
- Telomerase deficiency and dysfunctional telomeres in the lung tumor microenvironment impair tumor progression in NSCLC mouse models and patient-derived xenografts.Cell death and differentiation · 2023Article
- Senescent AECⅡ and the implication for idiopathic pulmonary fibrosis treatment.Frontiers in pharmacology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TRF1 is an essential component of the telomeric protective complex or shelterin. We previously showed that dysfunctional telomeres in alveolar type II (ATII) cells lead to interstitial lung fibrosis. Here, we study the lung pathologies upon telomere dysfunction in fibroblasts, club and basal cells. TRF1 deficiency in lung fibroblasts, club and basal cells induced telomeric damage, proliferative defects, cell cycle arrest and apoptosis. While Trf1 deletion in fibroblasts does not spontaneously lead to lung pathologies, upon bleomycin challenge exacerbates lung fibrosis. Unlike in females, Trf1 deletion in club and basal cells from male mice resulted in lung inflammation and airway remodeling. Here, we show that depletion of TRF1 in fibroblasts, Club and basal cells does not lead to interstitial lung fibrosis, underscoring ATII cells as the relevant cell type for the origin of interstitial fibrosis. Our findings contribute to a better understanding of proper telomere protection in lung tissue homeostasis.
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.