ArticleJCI insight2018
mTOR pathway activation drives lung cell senescence and emphysema.
Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers, 1 of them a synthesis 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
127 citing papers in PubMed, 1 synthesis or guideline pooled it, 208 citations in OpenAlex.
- Peripheral blood microbial signatures in current and former smokers.Scientific reports · 2021Pooled it
- Multi-omics study to elucidate molecular mechanism of polyhexamethylene guanidine phosphate (PHMG-p)-induced pulmonary damage in mice.Archives of toxicology · 2026Article
- Bone aging: a paradigm of multiscale degeneration and targeted rejuvenation.Bone research · 2026Review
- Eosinophil biology in COPD: from scientific insight to clinical treatment action.ERJ open research · 2026Review
- Fueling the fire: metabolic dysfunction and senescence as drivers of lung aging and disease.Physiological reviews · 2026Review
- Article
- Hallmarks of the ageing lung: 10 years later.The European respiratory journal · 2026Review
- Regenerative therapeutics for chronic obstructive pulmonary disease.Pharmacological reviews · 2026Review
- Lung mTOR activation leads to lung fibrosis or emphysema via senescence of specific lung cells.Scientific reports · 2026Article
- The mTOR Inhibitor Rapamycin Attenuates Ozone-Induced Airway Inflammation and Emphysema In Mice.Journal of inflammation research · 2026Article
- Precision geronutrition: personalized nutritional strategies to extend healthy lifespan.BMB reports · 2026Review
- Emerging Mechanistic Links Between Fucosylation and Senescence in Lung Diseases.Journal of respiratory biology and translational medicine · 2026Article
- Cellular plasticity and regenerative mechanisms in the lung.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- The Microbial Metabolite IDA Sensitizes Tumor Cells to ARF1 Inhibition by Inducing SVIL-dependent Senescence.International journal of biological sciences · 2026Article
- Aging and lung diseases: Unraveling mechanisms and therapeutic targets.Chinese medical journal pulmonary and critical care medicine · 2025Review
- Cellular senescence and cell therapy in cardiovascular diseases.Stem cell research & therapy · 2025Review
- mTOR dysregulation induces IL-6 and paracrine AT2 cell senescence impeding lung repair in lymphangioleiomyomatosis.Nature communications · 2025Article
- Mesenchymal stromal cell extracellular vesicles reduceAmerican journal of physiology. Lung cellular and molecular physiology · 2025Article
- NGAL knockdown alleviated CSE-induced cellular senescence and reduced MMP2 and MMP9 expression in alveolar macrophages through the PI3K/Akt pathway.European journal of medical research · 2025Article
- Virus-Induced Cellular Senescence Causes Pulmonary Sequelae Post-Influenza Infection.Aging cell · 2025Article
67 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
22 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic obstructive pulmonary disease (COPD) is a highly prevalent and devastating condition for which no curative treatment is available. Exaggerated lung cell senescence may be a major pathogenic factor. Here, we investigated the potential role for mTOR signaling in lung cell senescence and alterations in COPD using lung tissue and derived cultured cells from patients with COPD and from age- and sex-matched control smokers. Cell senescence in COPD was linked to mTOR activation, and mTOR inhibition by low-dose rapamycin prevented cell senescence and inhibited the proinflammatory senescence-associated secretory phenotype. To explore whether mTOR activation was a causal pathogenic factor, we developed transgenic mice exhibiting mTOR overactivity in lung vascular cells or alveolar epithelial cells. In this model, mTOR activation was sufficient to induce lung cell senescence and to mimic COPD lung alterations, with the rapid development of lung emphysema, pulmonary hypertension, and inflammation. These findings support a causal relationship between mTOR activation, lung cell senescence, and lung alterations in COPD, thereby identifying the mTOR pathway as a potentially new therapeutic target in COPD.
Indexed as
Identifiers
What Socratic 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 Socratic graph.