ArticleAmerican journal of respiratory cell and molecular biology2013
Lysophosphatidic acid receptor-2 deficiency confers protection against bleomycin-induced lung injury and fibrosis in mice.
Article in American journal of respiratory cell and molecular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.
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Who cites it
53 citing papers in PubMed, 1 synthesis or guideline pooled it, 107 citations in OpenAlex.
- Molecular Systems Architecture of Fibrotic Lung Microenvironment in Idiopathic Pulmonary Fibrosis.Cells · 2026Pooled it
- Serum metabolic profiling identified a distinct metabolic signature in patients with idiopathic pulmonary fibrosis - a potential biomarker role for LysoPC.Respiratory research · 2018Trial
- Insights into the binding mechanism and structural requirements of LPAR2 antagonists as antifibrotic agents based on homology modeling, molecular docking, prediction of membrane permeability and 3D QSAR.Journal of computer-aided molecular design · 2026Article
- Lysophosphatidic acid mediates skeletal muscle fibrosis in denervation via activation of YAP/TAZ.JCI insight · 2026Article
- Decoding lysophosphatidic acid signaling in physiology and disease: mapping the multimodal and multinodal signaling networks.Signal transduction and targeted therapy · 2025Review
- Phase 2 study design and analysis approach for BBT-877: an autotaxin inhibitor targeting idiopathic pulmonary fibrosis.BMJ open respiratory research · 2025Article
- Emerging pharmacological options in the treatment of idiopathic pulmonary fibrosis (IPF).Expert review of clinical pharmacology · 2024Review
- Functional meniscus reconstruction with biological and biomechanical heterogeneities through topological self-induction of stem cells.Bioactive materials · 2024Article
- The Role of Lysophospholipid Metabolites LPC and LPA in the Pathogenesis of Chronic Obstructive Pulmonary Disease.Metabolites · 2024Review
- Lysophosphatidic acid receptor 1 inhibition: a potential treatment target for pulmonary fibrosis.European respiratory review : an official journal of the European Respiratory Society · 2024Review
- Autotaxin inhibition attenuates the aortic valve calcification by suppressing inflammation-driven fibro-calcific remodeling of valvular interstitial cells.BMC medicine · 2024Article
- Review
- Integrating inflammatory biomarker analysis and artificial-intelligence-enabled image-based profiling to identify drug targets for intestinal fibrosis.Cell chemical biology · 2023Article
- A Protective Effect of Pirfenidone in Lung Fibroblast-Endothelial Cell Network via Inhibition of Rho-Kinase Activity.Biomedicines · 2023Article
- Emerging Roles of Lysophosphatidic Acid in Macrophages and Inflammatory Diseases.International journal of molecular sciences · 2023Review
- Lipid metabolism in idiopathic pulmonary fibrosis: From pathogenesis to therapy.Journal of molecular medicine (Berlin, Germany) · 2023Review
- Review
- Efficacy Comparison of LPAInternational journal of molecular sciences · 2022Article
- Long noncoding RNA ANRIL up-regulates CCND1 via sponging miR-98-5p to promote TGF-β1-induced human airway smooth muscle cell proliferation, migration, and extracellular matrix deposition.The Kaohsiung journal of medical sciences · 2022Article
- A Trans-Agency Workshop on the Pathophysiology of Radiation-Induced Lung Injury.Radiation research · 2022Article
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Idiopathic pulmonary fibrosis is a devastating disease characterized by alveolar epithelial cell injury, the accumulation of fibroblasts/myofibroblasts, and the deposition of extracellular matrix proteins. Lysophosphatidic acid (LPA) signaling through its G protein-coupled receptors is critical for its various biological functions. Recently, LPA and LPA receptor 1 were implicated in lung fibrogenesis. However, the role of other LPA receptors in fibrosis remains unclear. Here, we use a bleomycin-induced pulmonary fibrosis model to investigate the roles of LPA2 in pulmonary fibrogenesis. In the present study, we found that LPA2 knockout (Lpar2(-/-)) mice were protected against bleomycin-induced lung injury, fibrosis, and mortality, compared with wild-type control mice. Furthermore, LPA2 deficiency attenuated the bleomycin-induced expression of fibronectin (FN), α-smooth muscle actin (α-SMA), and collagen in lung tissue, as well as levels of IL-6, transforming growth factor-β (TGF-β), and total protein in bronchoalveolar lavage fluid. In human lung fibroblasts, the knockdown of LPA2 attenuated the LPA-induced expression of TGF-β1 and the differentiation of lung fibroblasts to myofibroblasts, resulting in the decreased expression of FN, α-SMA, and collagen, as well as decreased activation of extracellular regulated kinase 1/2, Akt, Smad3, and p38 mitogen-activated protein kinase. Moreover, the knockdown of LPA2 with small interfering RNA also mitigated the TGF-β1-induced differentiation of lung fibroblasts. In addition, LPA2 deficiency significantly attenuated the bleomycin-induced apoptosis of alveolar and bronchial epithelial cells in the mouse lung. Together, our data indicate that the knockdown of LPA2 attenuated bleomycin-induced lung injury and pulmonary fibrosis, and this may be related to an inhibition of the LPA-induced expression of TGF-β and the activation and differentiation of fibroblasts.
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