ArticleAmerican journal of physiology. Lung cellular and molecular physiology2011
Partial pneumonectomy of telomerase null mice carrying shortened telomeres initiates cell growth arrest resulting in a limited compensatory growth response.
Article in American journal of physiology. Lung cellular and molecular physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 31 citations in OpenAlex.
- An Overview of the Role of Genetic factors in Idiopathic Pulmonary Fibrosis: Insights from Epidemiology to Prognosis.International journal of medical sciences · 2025Review
- The Genetic and Epigenetic Footprint in Idiopathic Pulmonary Fibrosis and Familial Pulmonary Fibrosis: A State-of-the-Art Review.Diagnostics (Basel, Switzerland) · 2022Review
- Insights into the Pathogenesis of Pulmonary Fibrosis from Genetic Diseases.American journal of respiratory cell and molecular biology · 2022Review
- Research Progress in the Molecular Mechanisms, Therapeutic Targets, and Drug Development of Idiopathic Pulmonary Fibrosis.Frontiers in pharmacology · 2022Review
- Article
- Telomere Dysfunction in Idiopathic Pulmonary Fibrosis.Frontiers in medicine · 2021Review
- Familial Interstitial Lung Disease.Seminars in respiratory and critical care medicine · 2020Review
- Telomere shortening activates TGF-β/Smads signaling in lungs and enhances both lipopolysaccharide and bleomycin-induced pulmonary fibrosis.Acta pharmacologica Sinica · 2018Article
- Telomerase Deficiency Causes Alveolar Stem Cell Senescence-associated Low-grade Inflammation in Lungs.The Journal of biological chemistry · 2015Article
- Understanding Idiopathic Interstitial Pneumonia: A Gene-Based Review of Stressed Lungs.BioMed research international · 2015Review
- Age dependence of lung mesenchymal stromal cell dynamics following pneumonectomy.Stem cells and development · 2013Article
- Lung cancer stem cells: progress and prospects.Cancer letters · 2013Review
- Genetic studies provide clues on the pathogenesis of idiopathic pulmonary fibrosis.Disease models & mechanisms · 2013Review
- Senescence in chronic obstructive pulmonary disease.Proceedings of the American Thoracic Society · 2012Review
- Telomerase deficiency does not alter bleomycin-induced fibrosis in mice.Experimental lung research · 2012Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Telomerase mutations and significantly shortened chromosomal telomeres have recently been implicated in human lung pathologies. Natural telomere shortening is an inevitable consequence of aging, which is also a risk factor for development of lung disease. However, the impact of shortened telomeres and telomerase dysfunction on the ability of lung cells to respond to significant challenge is still largely unknown. We have previously shown that lungs of late generation, telomerase null B6.Cg-Terc(tm1Rdp) mice feature alveolar simplification and chronic stress signaling at baseline, a phenocopy of aged lung. To determine the role telomerase plays when the lung is challenged, B6.Cg-Terc(tm1Rdp) mice carrying shortened telomeres and wild-type controls were subjected to partial pneumonectomy. We found that telomerase activity was strongly induced in alveolar epithelial type 2 cells (AEC2) of the remaining lung immediately following surgery. Eighty-six percent of wild-type animals survived the procedure and exhibited a burst of early compensatory growth marked by upregulation of proliferation, stress response, and DNA repair pathways in AEC2. In B6.Cg-Terc(tm1Rdp) mice carrying shortened telomeres, response to pneumonectomy was characterized by decreased survival, diminished compensatory lung growth, attenuated distal lung progenitor cell response, persistent DNA damage, and cell growth arrest. Overall, survival correlated strongly with telomere length. We conclude that functional telomerase and properly maintained telomeres play key roles in both long-term survival and the early phase of compensatory lung growth following partial pneumonectomy.
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