ArticleActa pharmaceutica Sinica. B2026
Curcumin ameliorates metabolic dysfunction-associated steatotic liver disease
Article in Acta pharmaceutica Sinica. B, 2026. 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
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
1 citing paper in PubMed.
- Syringin disrupts the DLAT/MYC axis to dampen TAM polarization and suppress hepatocellular carcinoma progression.Acta pharmaceutica Sinica. B · 2026Article
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
Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common chronic liver disease, posing public health risks from potential irreversible liver damage. Curcumin (Cur), a polyphenolic compound from Zingiberaceae and Araceae, exhibits antihyperlipidemic and insulin-sensitizing effects. However, its targets and mechanisms in MASLD remain unclear. This study aimed to identify the potential targets and mechanisms by which Cur ameliorates MASLD. Cur markedly improved metabolic disorders and inflammation in rats and reduced intracellular lipid accumulation in HepG2 cells, primary hepatocytes, and AML12 cells. TKFC was identified as a direct target of Cur which binds to TKFC at Val136 and Glu538, thereby activating it. Gene microarray screening showed that Cur down-regulated the mRNA expression of
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.