ArticleWorld journal of gastroenterology2026
Pristimerin ameliorates spasmolytic polypeptide-expressing metaplasia by modulating
Article in World journal of gastroenterology, 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.
- Glycolytic reprogramming in precancerous lesions of gastric cancer progression: pathogenesis and therapeutic potential.Frontiers in oncology · 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
backgroundSpasmolytic polypeptide-expressing metaplasia (SPEM) is a gastric precancerous lesion (GPL) with high malignant potential. The ethyl acetate extract of
aimTo investigate the therapeutic effects of pristimerin on SPEM and its underlying mechanisms.
methodsPristimerin was administered to high-dose tamoxifen-induced SPEM mice to assess its effects on pathological progression, glycolytic reprogramming, and
resultsPristimerin effectively ameliorated gastric mucosal damage and oxyntic atrophy induced by high-dose tamoxifen, suppressed the aberrant upregulation of key glycolytic regulators, SPEM-specific markers, and stem cell markers, and upregulated p57 expression. In tamoxifen-induced GES-1 cells, pristimerin exhibited comparable therapeutic effects. Crucially, glycolysis inhibition in GES-1 cells effectively ameliorated tamoxifen-induced SPEM-associated phenotypes. In gastric organoids,
conclusionPristimerin effectively ameliorates gastric mucosal pathological damage and oxyntic atrophy in high-dose tamoxifen-induced SPEM mice, and improves SPEM progression by modulating
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.