ReviewProceedings of the American Thoracic Society2011
Stress responses affecting homeostasis of the alveolar capillary unit.
Review in Proceedings of the American Thoracic Society, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Trial
- Immunomodulatory Role of Nutrients: How Can Pulmonary Dysfunctions Improve?Frontiers in nutrition · 2021Review
- The Contribution of Endothelial Dysfunction in Systemic Injury Subsequent to SARS-Cov-2 Infection.International journal of molecular sciences · 2020Review
- RTP801 Amplifies Nicotinamide Adenine Dinucleotide Phosphate Oxidase-4-Dependent Oxidative Stress Induced by Cigarette Smoke.American journal of respiratory cell and molecular biology · 2017Article
- The inhibitory mechanism of Cordyceps sinensis on cigarette smoke extract-induced senescence in human bronchial epithelial cells.International journal of chronic obstructive pulmonary disease · 2016Article
- Senescence in chronic obstructive pulmonary disease.Proceedings of the American Thoracic Society · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
The maintenance of the alveolar structure is required throughout life. To accomplish this goal, alveolar cells, including endothelial, epithelial, and fibroblastic cells, provide key molecules with broad survival and antiapoptotic effects. These complex interactions are disrupted by cigarette smoke, leading to emphysema. Smoke imposes an environmental stress to the lung with the activation of "sensor-like" molecular signaling. Activation of RTP801, leading to mTOR inhibition, is paradigmatic of these responses. The accumulation of cellular damage, with the generation of endogenous mediators of inflammation, may proceed toward an aging phenotype. These alterations may impose significant challenges to cell-based regenerative or pharmacological therapies.
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.