ArticleGastroenterology2025
Fidaxomicin Reduces Collagen Expression in Intestinal Fibroblasts Via Platelet-Derived Growth Factor Receptor Beta and Glycogen Synthase Kinase-3 Beta Inhibition.
Article in Gastroenterology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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Who cites it
1 citing paper in PubMed.
- Cellular senescence in Crohn's disease: a double-edged sword in intestinal fibrosis.Frontiers in immunology · 2026Review
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Authors and funding
11 authors.
Funding
Abstract
BACKGROUND &
aimsAbout 30%-50% of patients with Crohn's disease (CD) eventually develop intestinal strictures, with intestinal fibrosis being a major component of them. There is currently no approved medication to treat fibrotic strictures.
methods10X Genomics Visium spatial RNA sequencing and high-throughput screening were used to discover the molecular targets of intestinal fibrosis. Stricturing Crohn's disease (CDS) patient-derived primary human intestinal fibroblasts (CD-HIFs), stricturing Crohn's disease patient-derived serum exosomes (CDSE), fresh surgically resected whole-thickness ileal tissues, and mouse models of intestinal fibrosis were used.
resultsSpatial RNA sequencing found overexpression of platelet-derived growth factor receptor beta (PDGFRB) in the fibrotic ileal tissues of CDS patients. PDGFRB small interfering RNA inhibited collagen expression in the CDSE-treated CD-HIFs. High-throughput screening identified PDGFRB inhibitors that suppressed collagen promoter activity in CDSE-treated CD-HIFs. A machine learning algorithm and molecular docking predicted PDGFR as a target for fidaxomicin. Fidaxomicin, a Food and Drug Administration-approved drug for Clostridioidesdifficile infection, inhibited collagen and PDGFRB messenger RNA (mRNA) expression in CDSE-treated CD-HIFs and CDS patient-derived ileal tissues. CDSE-treated CD-HIFs had increased PDGFRβ and glycogen synthase kinase-3 alpha/beta (GSK3ɑ/β) phosphorylation. Fidaxomicin inhibited PDGFRβ phosphorylation, PDGFRB mRNA expression, and GSK3β phosphorylation in CDSE-treated CD-HIFs. The antifibrogenic effect of fidaxomicin was attenuated by platelet-derived growth factor-BB (PDGF-BB) and insulin-like growth factor 1, which are a PDGFRβ ligand and a GSK3ɑ/β phosphorylation activator, respectively. In the SAMP1/YitFc mice, oral fidaxomicin treatment inhibited ileal fibrosis and ileal PDGFRB mRNA expression and PDGFRβ and GSK3β phosphorylation, which were abolished by Pdgfrb and Gsk3b overexpression.
conclusionsFidaxomicin inhibits intestinal fibrosis by reducing PDGFRβ phosphorylation and expression, GSK3β phosphorylation, and collagen expression in intestinal fibroblasts.
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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 Socratic graph.