ArticleAmerican journal of respiratory cell and molecular biology2016
Novel Mechanisms for the Antifibrotic Action of Nintedanib.
Article in American journal of respiratory cell and molecular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers, 2 of them syntheses that pooled it.
What it found
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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.
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.
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Who cites it
137 citing papers in PubMed, 2 syntheses or guidelines pooled it, 234 citations in OpenAlex.
- Targeted therapy for idiopathic pulmonary fibrosis: a bibliometric analysis of 2004-2024.Frontiers in medicine · 2025Pooled it
- Effectiveness of antifibrotics on health-related quality of life in patients with interstitial lung disease: a systematic review and meta-analysis.Therapeutic advances in respiratory diseasePooled it
- Targeting fibroblast activation suppresses chemotherapy-induced pro-invasive remodeling of the extracellular matrix.bioRxiv : the preprint server for biology · 2026Article
- β-carboline derivative Z86 alleviates pulmonary fibrosis via suppressing TGF-β/Smad signaling.Natural products and bioprospecting · 2026Article
- In Vitro Assessment of Nintedanib in Keratoconus Corneal Stromal Microenvironment.Biomolecules · 2026Article
- Erosive pustular dermatosis: Rapid clearance with nintedanib.JAAD case reports · 2026Article
- Regulated Cell Death in Idiopathic Pulmonary Fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Review
- Antifibrotic Drugs Regulate the Expression of Epithelial Sodium Channels in the Lungs.Advances in respiratory medicine · 2026Article
- Conditional BCL-2 Expression in Fibroblasts Promotes Persistent Pulmonary Fibrosis which is Reversible by Therapeutic BCL-2 Inhibition.Nature communications · 2026Article
- Effects of Nintedanib on Orofacial Fibroblasts and Myoblasts.Biomolecules · 2026Article
- The mechano-immunological barrier in fibrosis-associated lung cancer: targeting matrix stiffness and the Piezo1 axis for microenvironment normalization.Frontiers in pharmacology · 2026Review
- CD14Frontiers in immunology · 2026Article
- Targeting the neurovascular unit in retinal fibrosis: mechanisms and therapeutic perspectives.Frontiers in medicine · 2026Review
- Antifibrotics with Cross-Indication Potential: Challenges and Progress Towards a Universal Fibrosis-Modifying Therapy.Drug design, development and therapy · 2026Review
- Nintedanib induces rapid remission of steroid-resistant pulmonary fibrosis in an immunocompromised patient with recurrent COVID-19: A case report.Respiratory medicine case reports · 2026Article
- Understanding the Mechanisms Driving Fibrosis Following Cochlear Implantation-Lessons from Other Tissues.Cells · 2025Review
- Development and Validation of LC-MS/MS Method for Nintedanib and BIBF 1202 Monitoring in Plasma of Patients with Progressive Pulmonary Fibrosis Associated with Systemic Sclerosis.Pharmaceutics · 2025Article
- von Willebrand Factor Deficiency Inhibits Endothelial-to-Mesenchymal Transition to Attenuate Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2025Article
- Panax notoginseng saponins suppress the PI3K/AKT pathway to enhance autophagy and apoptosis in pulmonary fibrosis.Scientific reports · 2025Article
77 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a disease with relentless course and limited therapeutic options. Nintedanib (BIBF-1120) is a multiple tyrosine kinase inhibitor recently approved by the U.S. Food and Drug Administration for the treatment of IPF. The precise antifibrotic mechanism(s) of action of nintedanib, however, is not known. Therefore, we studied the effects of nintedanib on fibroblasts isolated from the lungs of patients with IPF. Protein and gene expression of profibrotic markers were assessed by Western immunoblotting and real-time PCR. Autophagy markers and signaling events were monitored by biochemical assays, Western immunoblotting, microscopy, and immunofluorescence staining. Silencing of autophagy effector proteins was achieved with small interfering RNAs. Nintedanib down-regulated protein and mRNA expression of extracellular matrix (ECM) proteins, fibronectin, and collagen 1a1 while inhibiting transforming growth factor (TGF)-β1-induced myofibroblast differentiation. Nintedanib also induced beclin-1-dependent, ATG7-independent autophagy. Nintedanib's ECM-suppressive actions were not mediated by canonical autophagy. Nintedanib inhibited early events in TGF-β signaling, specifically tyrosine phosphorylation of the type II TGF-β receptor, activation of SMAD3, and p38 mitogen-activated protein kinase. Nintedanib down-regulates ECM production and induces noncanonical autophagy in IPF fibroblasts while inhibiting TGF-β signaling. These mechanisms appear to be uncoupled and function independently to mediate its putative antifibrotic effects.
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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.