ReviewFrontiers in medicine2020
Senescence in Pulmonary Fibrosis: Between Aging and Exposure.
Review in Frontiers in medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- Common and rare variant analyses reveal genetic factors underlying idiopathic pulmonary fibrosis and its shared aetiology with severe COVID-19.EBioMedicine · 2025Pooled it
- Cellular hallmarks and aging clock of the human lung parenchyma.Nature communications · 2026Article
- A comprehensive review on the role of PM2.5 in modulating transplant immunity and graft survival.Particle and fibre toxicology · 2026Review
- Idiopathic Pulmonary Fibrosis: Cellular Heterogeneity, Mechanisms, and Therapeutic Implications.MedComm · 2025Review
- Aging affects reprogramming of pulmonary capillary endothelial cells after lung injury in male mice.Nature communications · 2025Article
- Inflammaging-Driven Osteoporosis: Is a Galectin-Targeted Approach Needed?International journal of molecular sciences · 2025Review
- Aging-associated interleukin-11 drives the molecular mechanism and targeted therapy of idiopathic pulmonary fibrosis.European journal of medical research · 2025Review
- Review
- Delineating excess comorbidities in idiopathic pulmonary fibrosis: an observational study.Respiratory research · 2024Observational
- Regenerative inflammation: When immune cells help to re-build tissues.The FEBS journal · 2024Review
- Environmental tobacco smoke exposure exaggerates bleomycin-induced collagen overexpression during pulmonary fibrogenesis.Journal of inflammation (London, England) · 2024Article
- Genetic and Pharmacological Inhibition of PAPP-A Reduces Bleomycin-Induced Pulmonary Fibrosis in Aged Mice via Reduced IGF Signaling.Aging biology · 2024Article
- Particulate matter composition drives differential molecular and morphological responses in lung epithelial cells.PNAS nexus · 2024Article
- The Effect ofJournal of experimental pharmacology · 2024Article
- Article
- TGF-β as A Master Regulator of Aging-Associated Tissue Fibrosis.Aging and disease · 2023Review
- Article
- Regulatory Cues in Pulmonary Fibrosis-With Emphasis on the AIM2 Inflammasome.International journal of molecular sciences · 2023Review
- MicroRNA profiling in dogs undergoing induced ischemic heart infarction: An experimental study.Veterinary world · 2023Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To date, chronic pulmonary pathologies represent the third leading cause of death in the elderly population. Evidence-based projections suggest that >65 (years old) individuals will account for approximately a quarter of the world population before the turn of the century. Genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication, are described as the nine "hallmarks" that govern cellular fitness. Any deviation from the normal pattern initiates a complex cascade of events culminating to a disease state. This blueprint, originally employed to describe aberrant changes in cancer cells, can be also used to describe aging and fibrosis. Pulmonary fibrosis (PF) is the result of a progressive decline in injury resolution processes stemming from endogenous (physiological decline or somatic mutations) or exogenous stress. Environmental, dietary or occupational exposure accelerates the pathogenesis of a senescent phenotype based on (1) window of exposure; (2) dose, duration, recurrence; and (3) cells type being targeted. As the lung ages, the threshold to generate an irreversibly senescent phenotype is lowered. However, we do not have sufficient knowledge to make accurate predictions. In this review, we provide an assessment of the literature that interrogates lung epithelial, mesenchymal, and immune senescence at the intersection of aging, environmental exposure and pulmonary fibrosis.
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.