ArticleRespiratory research2016
Pirfenidone and nintedanib modulate properties of fibroblasts and myofibroblasts in idiopathic pulmonary fibrosis.
Article in Respiratory research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
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Who cites it
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 125 citations in OpenAlex.
- Efficacy of antifibrotic drugs, nintedanib and pirfenidone, in treatment of progressive pulmonary fibrosis in both idiopathic pulmonary fibrosis (IPF) and non-IPF: a systematic review and meta-analysis.BMC pulmonary medicine · 2021Pooled it
- Safety of nintedanib added to pirfenidone treatment for idiopathic pulmonary fibrosis.The European respiratory journal · 2018Trial
- Effects of Nintedanib on Orofacial Fibroblasts and Myoblasts.Biomolecules · 2026Article
- Beyond attenuation: a translational review of curative-intent pharmacological targets in idiopathic pulmonary fibrosis.Frontiers in medicine · 2026Review
- A multimorphic variant in ThPOK causes an inborn error of immunity with T cell defects and fibrosis.The Journal of experimental medicine · 2025Article
- Patient Profile-Based Management with Nintedanib in Patients with Idiopathic Pulmonary Fibrosis.Pulmonary therapy · 2024Review
- The evolution ofEuropean respiratory review : an official journal of the European Respiratory Society · 2024Review
- Safety and tolerability of combination treatment with pirfenidone and nintedanib in patients with idiopathic pulmonary fibrosis: a systematic review and meta-analysis.Journal of thoracic disease · 2023Article
- Impact of ILD-Specific Therapies on Perioperative Course in Patients with Progressive Interstitial Lung Disease Undergoing Lung Transplantation.Journal of clinical medicine · 2023Article
- Article
- BAL Transcriptomes Characterize Idiopathic Pulmonary Fibrosis Endotypes With Prognostic Impact.Chest · 2022Article
- Article
- Novel Synthetic Polymer-Based 3D Contraction Assay: A Versatile Preclinical Research Platform for Fibrosis.ACS applied materials & interfaces · 2022Article
- Therapeutic Options for Systemic Sclerosis: Current and Future Perspectives in Tackling Immune-Mediated Fibrosis.Biomedicines · 2022Review
- COX-2/sEH Dual Inhibitor PTUPB Attenuates Epithelial-Mesenchymal Transformation of Alveolar Epithelial CellsOxidative medicine and cellular longevity · 2022Article
- Evaluation of nintedanib as a new postoperative antiscarring agent in experimental extraocular muscle surgery.International journal of ophthalmology · 2022Article
- Low Molecular Weight Fucoidan Inhibits Pulmonary Fibrosis In Vivo and In Vitro via Antioxidant Activity.Oxidative medicine and cellular longevity · 2022Article
- Network Pharmacology Prediction and Molecular Docking-Based Strategy to Discover the Potential Pharmacological Mechanism of Wen-Yu-Jin against Pulmonary Fibrosis in a Mouse Model.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Upcoming treatments for morphea.Immunity, inflammation and disease · 2021Review
- Pathological Roles and Clinical Usefulness of Periostin in Type 2 Inflammation and Pulmonary Fibrosis.Biomolecules · 2021Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIdiopathic pulmonary fibrosis (IPF) is an incurable lung disease with a poor prognosis. Fibroblasts and myofibroblasts are the key cells in the fibrotic process. Recently two drugs, pirfenidone and nintedanib, were approved for clinical use as they are able to slow down the disease progression. The mechanisms by which these two drugs act in in vitro cell systems are not known. The aim of this study was therefore to examine the effects of pirfenidone and nintedanib on fibroblasts and myofibroblasts structure and function established from patients with or without IPF.
methodsStromal cells were collected and cultured from control lung (n = 4) or IPF (n = 7). The cells were treated with pirfenidone and/or nintedanib and the effect of treatment was evaluated by measuring cell proliferation, alpha smooth muscle actin (α-SMA) and fibronectin expression by Western analysis and/or immunoelectron microscopy, ultrastructural properties by transmission electron microscopy and functional properties by collagen gel contraction and invasion assays.
resultsBoth pirfenidone and nintedanib reduced in vitro proliferation of fibroblastic cells in a dose dependent manner. The number of cells from control lung was reduced to 47 % (p = 0.04) and of IPF cells to 42 % (p = 0.04) by 1 mM pirfenidone and correspondingly to 67 % (p = 0.04) and 68 % (p = 0.04), by 1 μM nintedanib. If both drugs were used together, a further reduced proliferation was observed. Both pirfenidone and nintedanib were able to reduce the amount of α-SMA and the myofibroblastic appearance although the level of reduction was cell line dependent. In functional assays, the effect of both drugs was also variable.
conclusionsWe conclude that the ultrastructure and function of fibroblasts and myofibroblasts are affected by pirfenidone and nintedanib. Combination of the drugs reduced cell proliferation more than either of them individually. Human lung derived cell culture systems represent a potential platform for screening and testing drugs for fibrotic diseases.
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