ReviewFrontiers in medicine2018
Idiopathic Pulmonary Fibrosis: Aging, Mitochondrial Dysfunction, and Cellular Bioenergetics.
Review in Frontiers in medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 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
96 citing papers in PubMed, 1 synthesis or guideline pooled it, 150 citations in OpenAlex.
- Mammalian Neuraminidases in Immune-Mediated Diseases: Mucins and Beyond.Frontiers in immunology · 2022Pooled it
- Low Dose Carbon Monoxide Exposure in Idiopathic Pulmonary Fibrosis Produces a CO Signature Comprised of Oxidative Phosphorylation Genes.Scientific reports · 2019Trial
- Plasma SH Concentrations and Mortality in Patients with Newly Diagnosed Idiopathic Pulmonary Fibrosis.Antioxidants (Basel, Switzerland) · 2026Article
- Article
- Cellular Senescence: Emerging Therapeutic Target for Idiopathic Pulmonary Fibrosis Pathogenic Mechanisms and Therapeutic Strategies.Biomolecules & therapeutics · 2026Review
- Regulated Cell Death in Idiopathic Pulmonary Fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- ATF5 reduces LPS-induced cardiac injury by modulating pyroptosis via mitophagy.Journal of bioenergetics and biomembranes · 2026Article
- Molecular and Structural Changes, and Skeletal Muscle Strength and Endurance in Chronic Obstructive Pulmonary Disease and Interstitial Lung Disease: Practical Applications of Assessment and Management.Bioengineering (Basel, Switzerland) · 2026Review
- Decreased Complex I Activity in Blood lymphocytes Correlates with Idiopathic Pulmonary Fibrosis Severity.Biochemical genetics · 2026Article
- Mitochondrial stress response in lung cells triggered by the inhaled nanoplastics.Archives of toxicology · 2026Review
- Alternative Polyadenylation Contributes to Fibroblast Senescence in Pulmonary Fibrosis.Aging cell · 2025Article
- Sex-specific genetic effects on susceptibility to idiopathic pulmonary fibrosis.ERJ open research · 2025Article
- A Simple Ratio in a Complex Disease: Exploring the Neutrophil-to-Lymphocyte Ratio in Idiopathic Pulmonary Fibrosis.Journal of clinical medicine · 2025Review
- Aging-associated interleukin-11 drives the molecular mechanism and targeted therapy of idiopathic pulmonary fibrosis.European journal of medical research · 2025Review
- Article
- PGC-1α mediates migrasome secretion accelerating macrophage-myofibroblast transition and contributing to sepsis-associated pulmonary fibrosis.Experimental & molecular medicine · 2025Article
- MitochondrialInternational journal of molecular sciences · 2025Article
- Current Understanding of Pulmonary Fibrosis: Pathogenesis, Diagnosis, and Therapeutic Approaches.Canadian respiratory journal · 2025Review
- SS-31: A promising therapeutic agent against bleomycin-induced pulmonary fibrosis in Mice.PloS one · 2025Article
- Regulation of the NLRP3 inflammasome by autophagy and mitophagy.Immunological reviews · 2025Review
36 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
4 authors at 2 institutions in 1 country.
Funding
Abstract
At present, the etiology of idiopathic pulmonary fibrosis (IPF) remains elusive. Over the past two decades, however, researchers have identified and described the underlying processes that result in metabolic dysregulation, metabolic reprogramming, and mitochondrial dysfunction observed in the cells of IPF lungs. Metabolic changes and mitochondrial dysfunction in IPF include decreased efficiency of electron transport chain function with increasing production of reactive oxygen species, decreased mitochondrial biogenesis, and impaired mitochondrial macroautophagy, a key pathway for the removal of dysfunctional mitochondria. Metabolic changes in IPF have potential impact on lung cell function, differentiation, and activation of fibrotic responses. These alterations result in activation of TGF-β and predispose to the development of pulmonary fibrosis. IPF is a disease of the aged, and many of these same bioenergetic changes are present to a lesser extent with normal aging, raising the possibility that these anticipated alterations in metabolic processes play important roles in creating susceptibility to the development of IPF. This review explores what is known regarding the cellular metabolic and mitochondrial changes that are found in IPF, and examines this body of literature to identify future research direction and potential points of intervention in the pathogenesis of IPF.
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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.