ArticleScientific reports2022
Nintedanib regulates intestinal smooth muscle hyperplasia and phenotype in vitro and in TNBS colitis in vivo.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Nintedanib Enhances the Antibacterial Activity of Bedaquiline Against Non-Tuberculous Mycobacteria: In vitro and in Mice Models.Infection and drug resistance · 2026Article
- Macrophage-Orchestrated Metabolic Sensing Drives IBD Pathogenesis: A Framework for Targeted Therapy.International journal of biological sciences · 2026Review
- Angiogenic Factors and Inflammatory Bowel Diseases.Biomedicines · 2025Review
- Fibroblast Heterogeneity in Inflammatory Bowel Disease.International journal of molecular sciences · 2024Review
- Muscular hyperplasia in Crohn's disease strictures: through thick and thin.American journal of physiology. Cell physiology · 2024Review
- Drugst.One - a plug-and-play solution for online systems medicine and network-based drug repurposing.Nucleic acids research · 2024Article
- Automated High-Throughput Live Cell Monitoring of Scratch Wound Closure.Biomedical engineering and computational biology · 2024Article
- Drugst.One - A plug-and-play solution for online systems medicine and network-based drug repurposing.ArXiv · 2023Article
- Antispasmodic and Anti-inflammatory Effects of Kratom Leaf Extract on Acetic Acid-induced Ulcerative Colitis in Mice.In vivo (Athens, Greece)Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic inflammation of the human intestine in Crohn's disease (CD) causes bowel wall thickening, which typically progresses to stricturing and a recurrent need for surgery. Current therapies have limited success and CD remains idiopathic and incurable. Recent evidence shows a key role of intestinal smooth muscle cell (ISMC) hyperplasia in stricturing, which is not targeted by current anti-inflammatory therapeutics. However, progression of idiopathic pulmonary fibrosis, resembling CD in pathophysiology, is controlled by the tyrosine kinase inhibitors nintedanib (NIN) or pirfenidone, and we investigated these drugs for their effect on ISMC. In a culture model of rat ISMC, NIN inhibited serum- and PDGF-BB-stimulated growth and cell migration, and promoted the differentiated phenotype, while increasing secreted collagen. NIN did not affect signaling through PDGF-Rβ or NFκB but did inhibit cytokine-induced expression of the pro-inflammatory cytokines IL-1β and TNFα, supporting a transcriptional level of control. In TNBS-induced colitis in mice, which resembles CD, NIN decreased ISMC hyperplasia as well as expression of TNFα and IL-1β, without effect in control animals. NIN also inhibited growth of human ISMC in response to human serum or PDGF-BB, which further establishes a broad range of actions of NIN that support further trial in human IBD.
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