ArticleInternational journal of molecular sciences2012
Fasudil, a Rho-kinase inhibitor, attenuates bleomycin-induced pulmonary fibrosis in mice.
Article in International journal of molecular sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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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.
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Who cites it
46 citing papers in PubMed, 91 citations in OpenAlex.
- From force to fate: Implications of mechanomemory in lung disease.Respiratory research · 2026Review
- The importance of mechanical forces in chronic respiratory diseases.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Inhibition of Rho GEFs attenuates pulmonary fibrosis through suppressing myofibroblast activation and reprogramming profibrotic macrophages.Cell death & disease · 2025Article
- Emerging pharmacological options in the treatment of idiopathic pulmonary fibrosis (IPF).Expert review of clinical pharmacology · 2024Review
- Role and targeting of the AGC kinase family in pulmonary fibrosis (Review).Experimental and therapeutic medicine · 2024Review
- Modelling and targeting mechanical forces in organ fibrosis.Nature reviews bioengineering · 2024Article
- Beyond epithelial damage: vascular and endothelial contributions to idiopathic pulmonary fibrosis.The Journal of clinical investigation · 2023Review
- A ROCK inhibitor suppresses the transforming growth factor-beta-2-induced endothelial-mesenchymal transition in Schlemm's canal endothelial cells.Scientific reports · 2023Article
- ROCK (RhoA/Rho Kinase) Activation in Atrial Fibrillation: Molecular Pathways and Clinical Implications.Current cardiology reviews · 2023Article
- Evaluating a Specific Dual ROCK Inhibitor against Bleomycin-Induced Idiopathic Pulmonary Fibrosis in Rats.ACS pharmacology & translational science · 2022Article
- Natural Product-Based Potential Therapeutic Interventions of Pulmonary Fibrosis.Molecules (Basel, Switzerland) · 2022Review
- Systemic Sclerosis: From Pathophysiology to Novel Therapeutic Approaches.Biomedicines · 2022Review
- Lung Pneumonitis and Fibrosis in Cancer Therapy: A Review on Cellular and Molecular Mechanisms.Current drug targets · 2022Review
- Mechanotransduction Regulates the Interplays Between Alveolar Epithelial and Vascular Endothelial Cells in Lung.Frontiers in physiology · 2022Review
- Pulmonary Stretch and Lung Mechanotransduction: Implications for Progression in the Fibrotic Lung.International journal of molecular sciences · 2021Review
- A Rho Kinase (ROCK) Inhibitor, Y-27632, Inhibits the Dissociation-Induced Cell Death of Salivary Gland Stem Cells.Molecules (Basel, Switzerland) · 2021Article
- Engineering Advanced In Vitro Models of Systemic Sclerosis for Drug Discovery and Development.Advanced biology · 2021Review
- Mechano-therapeutics: Targeting Mechanical Signaling in Fibrosis and Tumor Stroma.Pharmacology & therapeutics · 2020Review
- Evasion of apoptosis by myofibroblasts: a hallmark of fibrotic diseases.Nature reviews. Rheumatology · 2020Review
- Rho-Kinase 1/2 Inhibition Prevents Transforming Growth Factor-β-Induced Effects on Pulmonary Remodeling and Repair.Frontiers in pharmacology · 2020Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanisms underlying the pathogenesis of idiopathic pulmonary fibrosis (IPF) involve multiple pathways, such as inflammation, epithelial mesenchymal transition, coagulation, oxidative stress, and developmental processes. The small GTPase, RhoA, and its target protein, Rho-kinase (ROCK), may interact with other signaling pathways known to contribute to pulmonary fibrosis. This study aimed to determine the beneficial effects and mechanisms of fasudil, a selective ROCK inhibitor, on bleomycin-induced pulmonary fibrosis in mice. Our results showed that the Aschcroft score and hydroxyproline content of the bleomycin-treated mouse lung decreased in response to fasudil treatment. The number of infiltrated inflammatory cells in the bronchoalveolar lavage fluid (BALF) was attenuated by fasudil. In addition, fasudil reduced the production of transforming growth factor-β1 (TGF-β1), connective tissue growth factor (CTGF), alpha-smooth muscle actin (α-SMA), and plasminogen activator inhibitor-1 (PAI-1) mRNA and protein expression in bleomycin-induced pulmonary fibrosis. These findings suggest that fasudil may be a potential therapeutic candidate for the treatment of 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.