ReviewEuropean respiratory review : an official journal of the European Respiratory Society2024
Lysophosphatidic acid receptor 1 inhibition: a potential treatment target for pulmonary fibrosis.
Review in European respiratory review : an official journal of the European Respiratory Society, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed.
- 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
- LPA1-Induced EMT of Retinal Pigment Epithelial Cells Promotes Subretinal Fibrosis via USP1-Mediated Deubiquitination and Stabilization of ZEB1.Investigative ophthalmology & visual science · 2026Article
- Inhibition of runt related transcription factor 1 with Ro24-7429 improves lung function in experimental models of idiopathic pulmonary fibrosis.Scientific reports · 2026Article
- A tetrahedral framework DNA-based bioswitchable miR-26a-5p delivery system for idiopathic pulmonary fibrosis.Materials today. Bio · 2026Article
- Immunological mechanisms and therapeutic approaches in pulmonary fibrosis.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Design of a phase II randomised, double-blind, placebo-controlled, dose-finding trial of BI 1819479 in patients with idiopathic pulmonary fibrosis.ERJ open research · 2026Article
- Beyond attenuation: a translational review of curative-intent pharmacological targets in idiopathic pulmonary fibrosis.Frontiers in medicine · 2026Review
- Nerandomilast - A Multifrontal Therapeutic Approach to Lung Fibrosis.American journal of respiratory cell and molecular biology · 2025Article
- Decoding lysophosphatidic acid signaling in physiology and disease: mapping the multimodal and multinodal signaling networks.Signal transduction and targeted therapy · 2025Review
- Role of Growth Factors in the Pathogenesis of Systemic-Sclerosis-Associated Fibrosis.International journal of molecular sciences · 2025Review
- The LPAR1 antagonist, PIPE-791 produces antifibrotic effects in models of lung fibrosis.Respiratory research · 2025Article
- Clinical Insights and Therapeutic Strategies for the Treatment of Interstitial Lung Disease in Patients with Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis: Current Trends and Future Directions.Journal of clinical medicine · 2025Review
- Targeting Autotaxin and Lysophosphatidic Acid in Pulmonary Fibrosis: Admilparant's Positive Results Show Continued Promise.American journal of respiratory and critical care medicine · 2025Article
- Macrophage Polarization: Learning to Manage It 3.0.International journal of molecular sciences · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lysophosphatidic acid (LPA)-mediated activation of LPA receptor 1 (LPAR1) contributes to the pathophysiology of fibrotic diseases such as idiopathic pulmonary fibrosis (IPF) and systemic sclerosis (SSc). These diseases are associated with high morbidity and mortality despite current treatment options. The LPA-producing enzyme autotaxin (ATX) and LPAR1 activation contribute to inflammation and mechanisms underlying fibrosis in preclinical fibrotic models. Additionally, elevated levels of LPA have been detected in bronchoalveolar lavage fluid from patients with IPF and in serum from patients with SSc. Thus, ATX and LPAR1 have gained considerable interest as pharmaceutical targets to combat fibrotic disease and inhibitors of these targets have been investigated in clinical trials for IPF and SSc. The goals of this review are to summarise the current literature on ATX and LPAR1 signalling in pulmonary fibrosis and to help differentiate the novel inhibitors in development. The mechanisms of action of ATX and LPAR1 inhibitors are described and preclinical studies and clinical trials of these agents are outlined. Because of their contribution to numerous physiologic events underlying fibrotic disease, ATX and LPAR1 inhibition presents a promising therapeutic strategy for IPF, SSc and other fibrotic diseases that may fulfil unmet needs of the current standard of care.
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.