ReviewRedox biology2016
Redox mechanisms in age-related lung fibrosis.
Review in Redox biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed, 86 citations in OpenAlex.
- Activation of the impaired NAMPT/SIRT7/SOD2 axis restores alveolar progenitor cell renewal in idiopathic pulmonary fibrosis.The Journal of clinical investigation · 2026Article
- Chimeric Antigen Receptor T Cells as Living Therapeutics Targeting Senescence and Age-Related Diseases.Research (Washington, D.C.) · 2026Review
- Cellular senescence in Crohn's disease: a double-edged sword in intestinal fibrosis.Frontiers in immunology · 2026Review
- Redox Mechanisms Driving Skin Fibroblast-to-Myofibroblast Differentiation.Antioxidants (Basel, Switzerland) · 2025Article
- The histone demethylase KDM6B links obstructive sleep apnea to idiopathic pulmonary fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Curcumin mediates oxidative stress to play an anti-fibrotic role, focusing on liver, renal, myocardial and pulmonary fibrosis.Frontiers in pharmacology · 2025Review
- Aging Lung: Molecular Drivers and Impact on Respiratory Diseases-A Narrative Clinical Review.Antioxidants (Basel, Switzerland) · 2024Review
- A Redox-Shifted Fibroblast Subpopulation Emerges in the Fibrotic Lung.American journal of respiratory cell and molecular biology · 2024Article
- Inhibition of EZH2 mitigates peritoneal fibrosis and lipid precipitation in peritoneal mesothelial cells mediated by klotho.Renal failure · 2023Article
- Sohlh2 promotes pulmonary fibrosis via repression of p62/Keap1/Nrf2 mediated anti-oxidative signaling pathway.Cell death & disease · 2023Article
- The role of immunosuppressive myofibroblasts in the aging process and age-related diseases.Journal of molecular medicine (Berlin, Germany) · 2023Review
- The aged extracellular matrix and the profibrotic role of senescence-associated secretory phenotype.American journal of physiology. Cell physiology · 2023Review
- Extracellular vesicle-matrix interactions.Nature reviews. Materials · 2023Article
- A roadmap for developing and engineeringBiophysics reviews · 2023Review
- Advances in cellular senescence in idiopathic pulmonary fibrosis (Review).Experimental and therapeutic medicine · 2023Review
- Article
- Immunometabolism changes in fibrosis: from mechanisms to therapeutic strategies.Frontiers in pharmacology · 2023Review
- Extracellular HSP90α promotes cellular senescence by modulating TGF-β signaling in pulmonary fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- NADPH oxidase family proteins: signaling dynamics to disease management.Cellular & molecular immunology · 2022Review
- PLG nanoparticles target fibroblasts and MARCO+ monocytes to reverse multiorgan fibrosis.JCI insight · 2022Article
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 at 1 institution in 1 country.
Funding
Abstract
Redox signaling and oxidative stress are associated with tissue fibrosis and aging. Aging is recognized as a major risk factor for fibrotic diseases involving multiple organ systems, including that of the lung. A number of oxidant generating enzymes are upregulated while antioxidant defenses are deficient with aging and cellular senescence, leading to redox imbalance and oxidative stress. However, the precise mechanisms by which redox signaling and oxidative stress contribute to the pathogenesis of lung fibrosis are not well understood. Tissue repair is a highly regulated process that involves the interactions of several cell types, including epithelial cells, fibroblasts and inflammatory cells. Fibrosis may develop when these interactions are dysregulated with the acquisition of pro-fibrotic cellular phenotypes. In this review, we explore the roles of redox mechanisms that promote and perpetuate fibrosis in the context of cellular senescence and aging.
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.