ReviewInternational journal of molecular sciences2020
Lipid Mediators Regulate Pulmonary Fibrosis: Potential Mechanisms and Signaling Pathways.
Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 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
85 citing papers in PubMed, 174 citations in OpenAlex.
- METTL3 Promotes Lipid Deposition and Pulmonary Fibrosis by Destabilizing PLIN2 in a m6A-Dependent Manner.Journal of cellular and molecular medicine · 2026Article
- LC-MS/MS-Based Lipidomic Profiling Reveals the Regulatory Effect of Stemoninoamide on TGF-β1-Induced Myofibroblast Transition in HFL1 Cells.Journal of mass spectrometry : JMS · 2026Article
- Metabolomic profiling reveals distinct and shared biology in COPD and IPF.Metabolomics : Official journal of the Metabolomic Society · 2026Article
- Reorganization of Innate Immune Cell Lipid Profiles by Bioinspired Meroterpenoids to Limit Inflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Altered cholesterol immunometabolism activates the macrophage NLRP3-inflammasome in lung fibrosis.American journal of respiratory cell and molecular biology · 2026Article
- Review
- Krüppel-like factor 14 enhances fatty acid oxidation to combat pulmonary fibrosis.Respiratory research · 2026Article
- Review
- Lipid Metabolism and Obesity in Early Life: Drivers of Chronic Lung Disease From Development to Adulthood.Molecular nutrition & food research · 2026Review
- The metabolic code of pulmonary disease: from mechanisms to therapeutic opportunities.Breathe (Sheffield, England) · 2026Review
- FTIR imaging identifies alterations in lung tissue structure and biochemical composition in human idiopathic pulmonary fibrosis.Scientific reports · 2026Article
- Genome-wide Association Studies of the Pathogenic Sphingosine-1-Phosphate Gene in Ulcerative ColitisEndocrine, metabolic & immune disorders drug targets · 2026Article
- Identification of diagnostic and prognostic phospholipid biomarkers in idiopathic pulmonary fibrosis via machine learning and in vivo validation.Human genomics · 2025Article
- Altered Metabolism in Idiopathic Pulmonary Fibrosis.Journal of cellular physiology · 2025Review
- Integration of single-cell and bulk transcriptomics uncovers CHST6 as a shared pathogenic driver in idiopathic pulmonary fibrosis and lung cancer.APL bioengineering · 2025Article
- From Fibrosis to Malignancy: Mechanistic Intersections Driving Lung Cancer Progression.Cancers · 2025Review
- Molecular mechanisms of efferocytosis imbalance in the idiopathic pulmonary fibrosis microenvironment: from gene screening to dynamic regulation analysis.Biology direct · 2025Article
- Exploring the Influence of Metabolic Changes in Fibrotic Lung Diseases.Pulmonary circulation · 2025Review
- Alteration of Lipid Metabolism in Patients with IPF and Its Association with Disease Severity and Prognosis: A Case-Control Study.International journal of molecular sciences · 2025Observational
- Article
25 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 3 institutions in 1 country.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease of unknown etiology characterized by distorted distal lung architecture, inflammation, and fibrosis. The molecular mechanisms involved in the pathophysiology of IPF are incompletely defined. Several lung cell types including alveolar epithelial cells, fibroblasts, monocyte-derived macrophages, and endothelial cells have been implicated in the development and progression of fibrosis. Regardless of the cell types involved, changes in gene expression, disrupted glycolysis, and mitochondrial oxidation, dysregulated protein folding, and altered phospholipid and sphingolipid metabolism result in activation of myofibroblast, deposition of extracellular matrix proteins, remodeling of lung architecture and fibrosis. Lipid mediators derived from phospholipids, sphingolipids, and polyunsaturated fatty acids play an important role in the pathogenesis of pulmonary fibrosis and have been described to exhibit pro- and anti-fibrotic effects in IPF and in preclinical animal models of lung fibrosis. This review describes the current understanding of the role and signaling pathways of prostanoids, lysophospholipids, and sphingolipids and their metabolizing enzymes in the development of lung fibrosis. Further, several of the lipid mediators and enzymes involved in their metabolism are therapeutic targets for drug development to treat IPF.
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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.