ReviewLung2015
The Role of Aging in Idiopathic Pulmonary Fibrosis.
Review in Lung, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 37 citations in OpenAlex.
- Alternative Polyadenylation Contributes to Fibroblast Senescence in Pulmonary Fibrosis.Aging cell · 2025Article
- Distinct lung functional, histological and cell senescence signatures in the single and repetitive bleomycin mouse models of idiopathic pulmonary fibrosis.Physiological reports · 2025Article
- The Hypoxia-Retinoid Axis in Idiopathic Pulmonary Fibrosis: Multifaceted Etiology and Therapeutic Potential.International journal of molecular sciences · 2025Review
- Aging, brain-derived neurotrophic factor, and allergen-induced pulmonary responses in mice.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- The Fibrotic Phenotype of Human Precision-Cut Lung Slices Is Maintained after Cryopreservation.Toxics · 2024Article
- Mesenchymal stem cells-extracellular vesicles alleviate pulmonary fibrosis by regulating immunomodulators.World journal of stem cells · 2024Article
- Clinicopathological Outlines of Post-COVID-19 Pulmonary Fibrosis Compared with Idiopathic Pulmonary Fibrosis.Biomedicines · 2023Review
- COVID-19-related end stage lung disease: two distinct phenotypes.Annals of medicine · 2022Article
- Cellular senescence is increased in airway smooth muscle cells of elderly persons with asthma.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- New Trends in Aging Drug Discovery.Biomedicines · 2022Review
- Review
- Emerging cellular and molecular determinants of idiopathic pulmonary fibrosis.Cellular and molecular life sciences : CMLS · 2021Review
- Review
- Cell senescence and fibrotic lung diseases.Experimental gerontology · 2020Review
- Ligustrazin increases lung cell autophagy and ameliorates paraquat-induced pulmonary fibrosis by inhibiting PI3K/Akt/mTOR and hedgehog signalling via increasing miR-193a expression.BMC pulmonary medicine · 2019Article
- Risk factors for the development of idiopathic pulmonary fibrosis: A review.Current pulmonology reports · 2018Article
- Serpine 1 induces alveolar type II cell senescence through activating p53-p21-Rb pathway in fibrotic lung disease.Aging cell · 2017Article
- Article
- Article
- Cellular senescence-like features of lung fibroblasts derived from idiopathic pulmonary fibrosis patients.Aging · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) has been gathering interest in recent years and as such this review will focus on the potential contributions that age plays on its onset and prevalence. Environmental stress over time caused by the inhalation of foreign substances results in subsequent damage and repair of lung tissue. This damage prematurely causes a decrease in stem cell differentiation potential. In conjunction with declining proliferation, the correlation between age and general attenuation of the immune system allows for the introduction of viral components such as the Epstein-Barr virus which has been associated with lung injury, a causation which has not yet been investigated. But, regardless of environmental factors, cellular alterations due to, or in correlation with, age could result in the onset or prolonging of IPF. General genetic mutation and epigenetic methylations accumulate over a person's lifespan while miRNA expression changes from birth to adulthood. This collection of alterations over time may cause dysregulation of expressed genetic material which can result in many age-related diseases including pulmonary fibrosis. Such alterations would be prevented by autophagy or cell-mediated apoptosis, but due to age-related dysregulations, these systems function at a diminished capacity. On the cellular level, the end result is an accumulation of dysfunctional organelles with damaged molecules, such as reactive oxygen species, and general genetic and epigenetic alterations resulting in excess generation of fibrous tissue and overall damage to the pulmonary system.
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.