ArticleScience translational medicine2011
β-arrestin deficiency protects against pulmonary fibrosis in mice and prevents fibroblast invasion of extracellular matrix.
Article in Science translational medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
What it found
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Who cites it
61 citing papers in PubMed, 90 citations in OpenAlex.
- Molecular imaging-guided discovery of a potent natural FAPα inhibitor for liver fibrosis therapy.Nature communications · 2026Article
- GPCR Biased Signaling in Cancer.Handbook of experimental pharmacology · 2026Review
- β-arrestin2: an emerging player and potential therapeutic target in inflammatory immune diseases.Acta pharmacologica Sinica · 2025Review
- Arrestin beta 1 Regulates Alveolar Progenitor Renewal and Lung Fibrosis.Journal of respiratory biology and translational medicine · 2024Article
- Administration of Gas6 attenuates lung fibrosis via inhibition of the epithelial-mesenchymal transition and fibroblast activation.Cell biology and toxicology · 2024Article
- Proteomics of severe SARS-COV-2 infection and paraquat poisoning in human lung tissue samples: comparison of microbial infected and toxic pulmonary fibrosis.Frontiers in cellular and infection microbiology · 2024Article
- β-Blockers in Hepatosplenic Schistosomiasis: A Narrative Review.The American journal of tropical medicine and hygiene · 2023Review
- Fibroblast Activation Protein Alpha (FAPα) in Fibrosis: Beyond a Perspective Marker for Activated Stromal Cells?Biomolecules · 2023Review
- SRC and TKS5 mediated podosome formation in fibroblasts promotes extracellular matrix invasion and pulmonary fibrosis.Nature communications · 2023Article
- Use of a pulmosphere model to evaluate drug antifibrotic responses in interstitial lung diseases.Respiratory research · 2023Article
- Reprogramming of cancer-associated fibroblasts by apoptotic cancer cells inhibits lung metastasis via Notch1-WISP-1 signaling.Cellular & molecular immunology · 2022Article
- HER2 drives lung fibrosis by activating a metastatic cancer signature in invasive lung fibroblasts.The Journal of experimental medicine · 2022Article
- Beta-blockers in patients with liver cirrhosis: Pragmatism or perfection?Frontiers in medicine · 2022Review
- Endothelial Cell Senescence Exacerbates Pulmonary Fibrosis Potentially Through Accelerated Endothelial to Mesenchymal Transition.The Kobe journal of medical sciences · 2021Article
- Protective Effects of Endothelin-2 Expressed in Epithelial Cells on Bleomycin-Induced Pulmonary Fibrosis in Mice.The Kobe journal of medical sciences · 2021Article
- Pro-inflammatory immunity supports fibrosis advancement in epidermolysis bullosa: intervention with Ang-(1-7).EMBO molecular medicine · 2021Article
- Molecular Signatures of Idiopathic Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2021Article
- β-Arrestin2 deficiency attenuates oxidative stress in mouse hepatic fibrosis through modulation of NOX4.Acta pharmacologica Sinica · 2021Article
- Gremlin2 Activates Fibroblasts to Promote Pulmonary Fibrosis Through the Bone Morphogenic Protein Pathway.Frontiers in molecular biosciences · 2021Article
- β-Arrestin2 is increased in liver fibrosis in humans and rodents.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
1 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
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Idiopathic pulmonary fibrosis is a progressive disease that causes unremitting extracellular matrix deposition with resulting distortion of pulmonary architecture and impaired gas exchange. β-Arrestins regulate G protein (heterotrimeric guanine nucleotide-binding protein)-coupled receptors through receptor desensitization while also acting as signaling scaffolds to facilitate numerous effector pathways. Here, we examine the role of β-arrestin1 and β-arrestin2 in the pathobiology of pulmonary fibrosis. In the bleomycin-induced mouse lung fibrosis model, loss of either β-arrestin1 or β-arrestin2 resulted in protection from mortality, inhibition of matrix deposition, and protected lung function. Fibrosis was prevented despite preserved recruitment of inflammatory cells and fibroblast chemotaxis. However, isolated lung fibroblasts from bleomycin-treated β-arrestin-null mice failed to invade extracellular matrix and displayed altered expression of genes involved in matrix production and degradation. Furthermore, knockdown of β-arrestin2 in fibroblasts from patients with idiopathic pulmonary fibrosis attenuated the invasive phenotype. These data implicate β-arrestins as mediators of fibroblast invasion and the development of pulmonary fibrosis, and as a potential target for therapeutic intervention in patients with idiopathic pulmonary fibrosis.
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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.