ArticleThe journals of gerontology. Series A, Biological sciences and medical sciences2016
Senescent Cells Contribute to the Physiological Remodeling of Aged Lungs.
Article in The journals of gerontology. Series A, Biological sciences and medical sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
What it found
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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.
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Who cites it
60 citing papers in PubMed, 88 citations in OpenAlex.
- Fueling the fire: metabolic dysfunction and senescence as drivers of lung aging and disease.Physiological reviews · 2026Review
- Substrate Stiffness and Viscoelasticity Influence Fibroblast Senescence.Journal of biomedical materials research. Part A · 2026Article
- Hallmarks of the ageing lung: 10 years later.The European respiratory journal · 2026Review
- Review
- SenSet defines cell-type specific senescence signatures in the aged human lung.The EMBO journal · 2026Article
- Review
- Lung mTOR activation leads to lung fibrosis or emphysema via senescence of specific lung cells.Scientific reports · 2026Article
- Cancer-cell-secreted DDAH1 induces TGF-β1/Smad3 signaling pathway to promote fibrosis and aging in lung.Nature aging · 2026Article
- Organoid: a promising solution to current challenges in cancer immunotherapy.npj biomedical innovations · 2025Review
- Increased substrate stiffness disrupts nuclear-cytoskeletal mechanical coupling in senescent cells.Materials today. Bio · 2025Article
- Stromal senescence contributes to age-related increases in cancer.Nature reviews. Cancer · 2025Review
- Deletion of PTHrP nuclear localization sequence and carboxyl terminus leads to lung dysplasia.Scientific reports · 2025Article
- Senotherapy for chronic lung disease.Pharmacological reviews · 2025Review
- Hyperoxia-induced senescence in fetal airway smooth muscle cells: role of mitochondrial reactive oxygen species and endoplasmic reticulum stress.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Lung endothelial cell senescence impairs barrier function and promotes neutrophil adhesion and migration.GeroScience · 2025Article
- Aging, brain-derived neurotrophic factor, and allergen-induced pulmonary responses in mice.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Targeting senescent cells in aging and COVID-19: from cellular mechanisms to therapeutic opportunities.Cell regeneration (London, England) · 2024Review
- Endoplasmic reticulum stress-induced senescence in human lung fibroblasts.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Involvement of Matricellular Proteins in Cellular Senescence: Potential Therapeutic Targets for Age-Related Diseases.International journal of molecular sciences · 2024Review
- Fibroblast senescence-associated extracellular matrix promotes heterogeneous lung niche.APL bioengineering · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
Abstract
Age-associated decline in organ function governs life span. We determined the effect of aging on lung function and cellular/molecular changes of 8- to 32-month old mice. Proteomic analysis of lung matrix indicated significant compositional changes with advanced age consistent with a profibrotic environment that leads to a significant increase in dynamic compliance and airway resistance. The excess of matrix proteins deposition was associated modestly with the activation of myofibroblasts and transforming growth factor-beta signaling pathway. More importantly, detection of senescent cells in the lungs increased with age and these cells contributed toward the excess extracellular matrix deposition observed in our aged mouse model and in elderly human samples. Mechanistic target of rapamycin (mTOR)/AKT activity was enhanced in aged mouse lungs compared with those from younger mice associated with the increased expression of the histone variant protein, MH2A, a marker for aging and potentially for senescence. Introduction in the mouse diet of rapamycin, significantly blocked the mTOR activity and limited the activation of myofibroblasts but did not result in a reduction in lung collagen deposition unless it was associated with prevention of cellular senescence. Together these data indicate that cellular senescence significantly contributes to the extracellular matrix changes associated with aging in a mTOR 1-dependent mechanism.
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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.