Synapse
⌘+K
Synapse
PulseExploreClubsResearchersJournals
Instagram
HomeClubsExplore
January 23, 2026Journal of Crohn s and Colitis

P0087Targeting TRPM8 as a novel strategy to mitigate intestinal fibrosis in Crohn’s Disease.

View Full Paper
Ask AI
Bookmark
Share

Authors

MNM NaniMRM M RinaldiMMMaría Cruz Miraglia

Discussion

Loading...

Member takes

Overview

Investigates TRPM8's role in intestinal fibrosis, implying its potential as a therapeutic target.

Key Points

  • The aim is to explore how TRPM8 influences intestinal fibrosis in Crohn's disease.
  • Analyzed human intestinal biopsies for TRPM8 expression in fibrotic and non-fibrotic tissues.
  • Characterized primary intestinal fibroblasts from fibrotic patients using RT-PCR for fibrotic markers.
  • Established a TNBS-induced murine model of intestinal fibrosis, treated with TRPM8 antagonist AMTB (10 mg/kg).
  • Evaluated fibrosis progression through colonoscopy, qRT-PCR, and histological analyses.
  • Characterized immune signaling using flow cytometry for CX3CR1+ cells.
  • TRPM8 expression was significantly higher in fibrotic biopsies compared to healthy tissues.
  • Treatment with AMTB altered the proliferative behavior of primary human intestinal fibroblasts.
  • AMTB treatment reduced intestinal fibrosis in vivo, assessed by various metrics including colon weight/length ratio and histological evaluation.
  • Flow cytometry showed AMTB modulation of CX3CR1+ immune cell populations in the colon.
  • Isolated fibroblasts from treated mice showed reduced expression of inflammatory and fibrotic markers.

Cite This Study

Nani et al. (2026) studied this question.

synapsesocial.com/papers/69730f78c8125b09b0d1f4c6https://doi.org/10.1093/ecco-jcc/jjaf231.268
View Full Paper
Ask AI
Bookmark
Share