ReviewFrontiers in medicine2018
Autotaxin in Pathophysiology and Pulmonary Fibrosis.
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 72 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
72 citing papers in PubMed, 1 synthesis or guideline pooled it, 133 citations in OpenAlex.
- Blood gene expression risk profiles and interstitial lung abnormalities: COPDGene and ECLIPSE cohort studies.Respiratory research · 2022Pooled it
- Safety, Pharmacokinetics, and Pharmacodynamics of the Autotaxin Inhibitor GLPG1690 in Healthy Subjects: Phase 1 Randomized Trials.Journal of clinical pharmacology · 2019Trial
- Context-dependent lysophosphatidic acid signalling in inflammation: evidence hierarchy, myeloid regulation and translational gaps.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- An aerosolized dual-action autotaxin inhibitor-PPARγ agonist for the treatment of pulmonary fibrosis.Cell reports. Medicine · 2026Article
- STL1267 inhibits myofibroblast differentiation in a TGFβ1-driven human lung fibroblast model.American journal of physiology. Cell physiology · 2026Article
- Inhibition of interleukin-1 receptor-associated kinase (IRAK)-4 provides partial rescue of interleukin-1 beta induced functional and gene expression changes in equine tenocytes.Molecular biology reports · 2025Article
- Lpar5 regulates the CD8 T-cell response to persistent virus infection by altering exhaustion programming, survival, and NK receptor expression.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Age-related diseases as a testbed for anti-aging therapeutics: the case of idiopathic pulmonary fibrosis.Aging · 2025Review
- Emerging Concepts in Therapeutic Interventions for Idiopathic Pulmonary Fibrosis.Seminars in respiratory and critical care medicine · 2025Review
- Integrated multiomics of pressure overload in the human heart prioritizes targets relevant to heart failure.Nature communications · 2025Article
- Dysregulated ATX-LPA and YAP/TAZ signaling in dystrophic SgcdSkeletal muscle · 2025Article
- Advances in idiopathic pulmonary fibrosis diagnosis and treatment.Chinese medical journal pulmonary and critical care medicine · 2025Review
- Structure-Based Discovery of MolPort-137: A Novel Autotaxin Inhibitor That Improves Paclitaxel Efficacy.International journal of molecular sciences · 2025Article
- The role of vascularity and the fibrovascular interface in interstitial lung diseases.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Single-cell analysis reveals the loss of FABP4-positive proliferating valvular endothelial cells relates to functional mitral regurgitation.BMC medicine · 2024Article
- Immune mechanisms and novel therapies for idiopathic pulmonary fibrosis.Pharmaceutical science advances · 2024Review
- Article
- Pharmacological treatment in Idiopathic Pulmonary Fibrosis: current issues and future perspectivesMultidisciplinary respiratory medicine · 2024Article
- Linking the Autotaxin-LPA Axis to Medicinal Cannabis and the Endocannabinoid System.International journal of molecular sciences · 2024Review
- Dysregulated autotaxin expression by T cells in multiple sclerosis.Journal of neuroimmunology · 2024Article
12 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
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lysophospholipid signaling is emerging as a druggable regulator of pathophysiological responses, and especially fibrosis, exemplified by the relative ongoing clinical trials in idiopathic pulmonary fibrosis (IPF) patients. In this review, we focus on ectonucleotide pyrophosphatase-phosphodiesterase 2 (ENPP2), or as more widely known Autotaxin (ATX), a secreted lysophospholipase D (lysoPLD) largely responsible for extracellular lysophosphatidic acid (LPA) production. In turn, LPA is a bioactive phospholipid autacoid, forming locally upon increased ATX levels and acting also locally through its receptors, likely guided by ATX's structural conformation and cell surface associations. Increased ATX activity levels have been detected in many inflammatory and fibroproliferative conditions, while genetic and pharmacologic studies have confirmed a pleiotropic participation of ATX/LPA in different processes and disorders. In pulmonary fibrosis, ATX levels rise in the broncheoalveolar fluid (BALF) and stimulate LPA production. LPA engagement of its receptors activate multiple G-protein mediated signal transduction pathways leading to different responses from pulmonary cells including the production of pro-inflammatory signals from stressed epithelial cells, the modulation of endothelial physiology, the activation of TGF signaling and the stimulation of fibroblast accumulation. Genetic or pharmacologic targeting of the ATX/LPA axis attenuated disease development in animal models, thus providing the proof of principle for therapeutic interventions.
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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 Socratic graph.