ArticlePediatric research2025
A two-hit model in biliary atresia: cooperative viral-bacterial activation of MMP7 via TLR4/NF-κB signaling.
Article in Pediatric research, 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Matrix stiffness may drive multi-cellular crosstalk via YAP signaling in biliary atresia liver fibrosis: a mechanistic review.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
impactRhesus rotavirus (RRV) infection primes biliary epithelial cells to respond hyperactively to low-dose lipopolysaccharide (LPS), triggering upregulation of matrix metalloproteinase-7 (MMP7) via TLR4/NF-κB signaling. Loss of endotoxin tolerance in biliary atresia (BA), associated with reduced expression of IRAK-M, leads to uncontrolled inflammation and tissue damage. MMP7 acts as a dual-function molecule, contributing to both extracellular matrix remodeling and amplification of inflammatory signaling in BA. Targeting the TLR4/NF-κB/MMP7 signaling axis represents a promising therapeutic strategy with potential applications in disease modification and early diagnosis of BA.
Indexed as
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Registered trials
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 OpenQuestion graph.