Synapse
⌘+K
Synapse
PulseExploreClubsResearchersJournals
Instagram
HomeClubsExplore
June 4, 2026Hepatology

Non-transcriptional activity of IRF3 promotes liver fibrosis and stress granule assembly via a dsRNA-TLR3-dependent pathway in hepatic stellate cells

View Full Paper
Ask AI
Bookmark
Share

Authors

JTJared TraversCleveland ClinicYZY ZhangCleveland ClinicCRChristina K. Cajigas‐Du RossCleveland Clinic

Discussion

Loading...

Member takes

Implication

Randomized trial demonstrates non-transcriptional IRF3 activity promotes liver fibrosis in mice, suggesting novel therapeutic targets.

Key Points

  • This research explores how the non-transcriptional functions of IRF3 influence liver fibrosis, particularly in hepatic stellate cells (HSCs).
  • Utilized chronic carbon tetrachloride (CCl4) models in C57BL/6J mice and Irf3 S1/S1 mutant mice.
  • Applied TGFβ stimulation in primary HSCs and LX2 cells to assess fibrogenic gene expression and collagen production.
  • Conducted proteomic analysis to identify stress granule-associated proteins in the IRF3 interactome.
  • CCl4-induced fibrosis occurred in wild-type and Irf3 S1/S1 mice but not Irf3 -/- mice, suggesting IRF3's critical role.
  • Primary HSCs from Irf3 -/- mice showed reduced fibrogenic gene expression upon TGFβ stimulation compared to those from Irf3 S1/S1 mice.
  • Endogenous dsRNA accumulation triggered IRF3-containing stress granule assembly, reliant on TLR3 signaling.

Cite This Study

Travers et al. (2026) studied this question.

synapsesocial.com/papers/6a2117bfd499ed480b17087ahttps://doi.org/10.1097/hep.0000000000001803
View Full Paper
Ask AI
Bookmark
Share