ArticleMolecular biology reports2026
Agmatine protects against MAFLD via decreasing RBM15/IGF2BP2-mediated m
Article in Molecular biology reports, 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
6 authors.
Funding
Abstract
backgroundGut microbiota and its metabolites are revealed to affect metabolic dysfunction-associated fatty liver disease (MAFLD) progression. Precedingly, we proved bifidobacterium bifidum BGN4 fractions declined sterol regulatory element-binding transcription factor 1 (SREBP1) to suppress ferroptosis during MAFLD. This study explored whether agmatine, a key metabolite induced by BGN4, affected MAFLD development.
methodsHigh-fat diet (HFD)-fed mice or palmitate (PA)-stimulated MIHA hepatocytes were treated with agmatine. General conditions of the mice were evaluated by behavioral tests, body weight, liver weight, and plasma biochemical parameters, while hepatic steatosis was observed with H&E staining. Hepatocyte cytotoxicity was assessed by lactate dehydrogenase assay, and mitochondrial dysfunction was evaluated with ATP content and oxygen consumption rate. Ferroptosis was estimated by lipid peroxidation, iron, and expressions of related proteins. Immunohistochemistry, immunofluorescence, western blot, and RT-qPCR were used for detecting protein and mRNA levels. Molecular mechanism was investigated using RNA immunoprecipitation, methylated RNA immunoprecipitation, luciferase reporter assay, and RNA stability assay.
resultsIn the HFD-induced MAFLD mouse model, agmatine treatment alleviated metabolic abnormalities, depression-related behavior, hepatic damage, and ferroptosis, and decreased Iba1 and GFAP in cortex. In the in vitro model of PA-induced hepatocytes, agmatine mitigates cytotoxicity, mitochondrial dysfunction, and ferroptosis. Increases of SREBP1, RNA binding motif protein 15 (RBM15), and IGF2 mRNA binding protein2 (IGF2BP2) in MAFLD models were rescued by agmatine. RBM15/IGF2BP2 knockdown inhibited m
conclusionAgmatine relieved MAFLD via inhibiting RBM15/IGF2BP2-mediated SREBP1 m
Indexed as
Identifiers
42183943What 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.