ArticleFrontiers in cell and developmental biology2026
Toll/IL-1 receptor domain-containing adaptor protein plays a crucial role in macrophage-mediated hepatic stellate cell activation in alcoholic liver disease.
Article in Frontiers in cell and developmental biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Alcoholic liver disease (ALD) remains a significant global health issue, marked by chronic liver injury and progressive accumulation of extracellular matrix (ECM), ultimately leading to fibrosis. A key driver of this fibrotic process is the activation of hepatic stellate cells (HSCs), largely influenced by inflammatory signals from immune cells-particularly macrophages. This study explores the specific signalling mechanisms in macrophages that contribute to HSC activation in the context of alcohol exposure, aiming to identify new therapeutic targets. Methods: To mimic the disease condition, THP-1-derived macrophages were stimulated with ethanol and lipopolysaccharide (LPS). Cytokine expression was quantified by RT-qPCR, while the activation of TIRAP, MAPKs, and fibrotic markers in THP-1-derived macrophages and LX-2 cells was evaluated by western blotting and immunofluorescence staining. Result: Activation was indicated by increased expression of pro-inflammatory and fibrogenic factors, including IL-1β, TNF-α, IL-6, TGF-β, and PDGF-α. Signalling analysis revealed heightened phosphorylation of TIRAP (Toll/IL-1 receptor domain-containing adaptor protein), along with activation of downstream MAPK pathways (p38, ERK, JNK) and NF-κB. The conditioned media from these activated macrophages was applied to HSC cultures, resulting in elevated levels of fibrotic markers such as α-smooth muscle actin (α-SMA) and collagen, confirming HSC activation. Importantly, silencing TIRAP in macrophages significantly reduced the expression of these markers in HSCs, suggesting a key role for TIRAP in driving fibrogenesis. Conclusion: Overall, these findings underscore the importance of TIRAP- mediated signalling in macrophages as a central mechanism in alcohol- induced liver fibrosis, and propose macrophage TIRAP as a promising target for therapeutic intervention in ALD.
Indexed as
Identifiers
What OpenQuestion holds
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.