ReviewThe American journal of pathology2026
Transforming Growth Factor-β Signaling in Alcohol-Associated Liver Disease: A Multicellular Perspective.
Review in The American journal of pathology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed.
- Hepatic, oxidative, and immunological alterations in adults with concomitant Schistosoma mansoni infection and alcohol abuse in an endemic area of Cameroon.BMC infectious diseases · 2026Article
- [Ethanol promotes oxaliplatin resistance in colorectal cancer by activating the TGF‑β/Smad/P21 signaling axis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Gut-Liver Axis Failure in Critical Alcohol-Associated Liver Disease: From ICU Secondary Hits to Microbiome-Targeted Therapy.Mediators of inflammation · 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transforming growth factor-β (TGF-β) signaling exerts broad regulatory effects on alcohol-associated liver disease (ALD) progression, influencing processes such as hepatocellular injury, regeneration, inflammation, fibrogenesis, cirrhosis, carcinogenesis, and hepatic failure. TGF-β modifies alcohol-induced signals in multiple liver-resident cell types, including hepatocytes, hepatic stellate cells, liver sinusoidal endothelial cells, and immune populations, particularly macrophages. To delineate its context-specific roles in ALD, 154 of 421 PubMed-listed publications (2000 to 2025; search terms TGF-β and alcohol and liver disease) were reviewed, supplemented by 19 foundational studies published earlier. In hepatocytes, TGF-β promotes oxidative stress, apoptosis, metabolic reprogramming, and epithelial-to-mesenchymal transition. In hepatic stellate cells and Kupffer cells, gut-derived endotoxins, ethanol, and unsaturated fatty acids induce TGF-β alongside proinflammatory cytokines. Ethanol metabolism generates acetaldehyde, which drives TGF-β and receptor expression, enhances canonical and noncanonical signaling, and engages epigenetic regulators to promote extracellular matrix deposition. In liver sinusoidal endothelial cells, alcohol-induced TGF-β suppresses proliferation, contributing to sinusoidal capillarization, impaired endothelial regeneration, and fibrogenesis. TGF-β dampens clearance of damaged hepatocytes and perpetuating chronic injury by suppressing natural killer cell cytotoxicity and promoting regulatory T-cell differentiation. At end-stage disease, TGF-β promotes expansion and fate switching of cholangiocyte-derived liver progenitor cells to replenish lost hepatocytes. Despite its central role in ALD, therapeutic exploitation of TGF-β signaling remains underexplored. Future studies should define cell type-specific signaling nodes to enable precision therapies.
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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.