ArticleHepatology communications2025
Ceramide kinase suppresses ferroptosis and protects against alcohol-associated liver disease through the p38 MAPK-HSPB1 pathway.
Article in Hepatology communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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
4 citing papers in PubMed.
- Article
- Article
- YTHDF1/SLC39A4 signaling axis promotes gastric cancer cell proliferation by suppressing cuproptosis ex vivo and in vitro.Cancer gene therapy · 2026Article
- Role of Ceramide Kinase/C1P in the Regulation of Cell Growth and Survival.International journal of molecular sciences · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlcohol-associated liver disease (ALD) is characterized by progressive liver injury, which is influenced by aberrant oxidative stress, ferroptosis, and sphingolipid metabolism. Although the inhibition of hepatic ceramide production has shown promise in ALD management, the specific roles of ceramide kinase (CERK) and its metabolite ceramide-1-phosphate in ALD pathogenesis and ferroptosis have not been fully explored.
methodsTo investigate the role of CERK in ALD, we established an alcohol-induced liver injury model using the Gao-binge protocol in C57BL/6 wild-type, Cerk knockout, and Cerk overexpression mice. The molecular mechanisms underlying CERK-regulated ALD were identified and characterized through liver transcriptomics and pharmacological inhibition of CERK.
resultsAlcohol consumption significantly increased the expression of CERK in the liver. Functional studies demonstrated that CERK mitigates alcohol-induced liver injury by attenuating oxidative stress and ferroptosis both in vivo and in vitro. Mechanistically, these effects were mediated through the activation of heat shock protein beta-1 via the p38 mitogen-activated protein kinase signaling pathway, highlighting HSPB1's role in suppressing oxidative stress and ferroptosis.
conclusionsOur findings indicated that enhancing CERK expression or activity may represent a novel therapeutic strategy for mitigating alcohol-induced liver injury. This approach could offer a promising avenue for treating ALD and its associated ferroptotic damage.
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.