ArticleJournal of cellular and molecular medicine2014
Lysophosphatidic acid accelerates lung fibrosis by inducing differentiation of mesenchymal stem cells into myofibroblasts.
Article in Journal of cellular and molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
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Who cites it
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.
- Mesenchymal Stromal Cells in Animal Bleomycin Pulmonary Fibrosis Models: A Systematic Review.Stem cells translational medicine · 2015Pooled it
- Metabolic Profiling Reveals Organ-Specific Molecular Pathologies and Aging-Associated Biomarkers in Progeroid Laminopathy.Smart medicine · 2026Article
- Circulating miR-378a-3p attenuates pulmonary inflammation and fibrosis via BAT-lung crosstalk.Journal of nanobiotechnology · 2026Article
- Gintonin as a Lysophosphatidic Acid-Enriched GPCR Ligand System: Molecular Architecture and Receptor Pharmacology inBiomolecules · 2026Review
- Decoding lysophosphatidic acid signaling in physiology and disease: mapping the multimodal and multinodal signaling networks.Signal transduction and targeted therapy · 2025Review
- Fibrotic Disease: from Signaling Pathways and Biomarkers to Molecular Imaging.Molecular imaging and biology · 2025Review
- Inhibition of autotaxin activity with IOA-289 decreases fibrosis in mouse E0771 breast tumors.International journal of cancer · 2025Article
- Causal Effects Between Genetically Determined Human Serum Metabolite Levels on the Risk of Idiopathic Pulmonary Fibrosis: A Mendelian Randomization Study.The clinical respiratory journal · 2025Article
- What Is on the Horizon for Treatments in Idiopathic Pulmonary Fibrosis?Journal of clinical medicine · 2024Review
- Lysophosphatidic Acid-Mediated Inflammation at the Heart of Heart Failure.Current cardiology reports · 2024Review
- Small-molecule-mediated OGG1 inhibition attenuates pulmonary inflammation and lung fibrosis in a murine lung fibrosis model.Nature communications · 2023Article
- Inhibition of LPA-LPAR1 and VEGF-VEGFR2 Signaling in IPF Treatment.Drug design, development and therapy · 2023Review
- Lung fibrogenic microenvironment in mouse reconstitutes human alveolar structure and lung tumor.iScience · 2022Article
- Odontogenic Differentiation-Induced Tooth Regeneration byCurrent issues in molecular biology · 2022Article
- Review
- Intestinal Fibrosis in Inflammatory Bowel Disease and the Prospects of Mesenchymal Stem Cell Therapy.Frontiers in immunology · 2022Review
- Preventing the Increase in Lysophosphatidic Acids: A New Therapeutic Target in Pulmonary Hypertension?Metabolites · 2021Article
- Revisiting the role of lysophosphatidic acid in stem cell biology.Experimental biology and medicine (Maywood, N.J.) · 2021Review
- Lysophosphatidic Acid Receptors: Biochemical and Clinical Implications in Different Diseases.Journal of Cancer · 2020Review
- Antifibrotic effects of 2-carba cyclic phosphatidic acid (2ccPA) in systemic sclerosis: contribution to the novel treatment.Arthritis research & therapy · 2019Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung fibrosis is characterized by vascular leakage and myofibroblast recruitment, and both phenomena are mediated by lysophosphatidic acid (LPA) via its type-1 receptor (LPA1). Following lung damage, the accumulated myofibroblasts activate and secrete excessive extracellular matrix (ECM), and form fibrotic foci. Studies have shown that bone marrow-derived cells are an important source of myofibroblasts in the fibrotic organ. However, the type of cells in the bone marrow contributing predominantly to the myofibroblasts and the involvement of LPA-LPA1 signalling in this is yet unclear. Using a bleomycin-induced mouse lung-fibrosis model with an enhanced green fluorescent protein (EGFP) transgenic mouse bone marrow replacement, we first demonstrated that bone marrow derived-mesenchymal stem cells (BMSCs) migrated markedly to the bleomycin-injured lung. The migrated BMSC contributed significantly to α-smooth muscle actin (α-SMA)-positive myofibroblasts. By transplantation of GFP-labelled human BMSC (hBMSC) or EGFP transgenic mouse BMSC (mBMSC), we further showed that BMSC might be involved in lung fibrosis in severe combined immune deficiency (SCID)/Beige mice induced by bleomycin. In addition, using quantitative-RT-PCR, western blot, Sircol collagen assay and migration assay, we determined the underlying mechanism was LPA-induced BMSC differentiation into myofibroblast and the secretion of ECM via LPA1. By employing a novel LPA1 antagonist, Antalpa1, we then showed that Antalpa1 could attenuate lung fibrosis by inhibiting both BMSC differentiation into myofibroblast and the secretion of ECM. Collectively, the above findings not only further validate LPA1 as a drug target in the treatment of pulmonary fibrosis but also elucidate a novel pathway in which BMSCs contribute to the pathologic process.
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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.