ArticleBMC pharmacology & toxicology2025
AMD1, a cardiotoxicity target for Maduramicin.
Article in BMC pharmacology & toxicology, 2025. 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
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe aim of this study was to investigate AMD1 cardiotoxicity function for Maduramicin (Mad).
methodsSD rats were divided into control (Control) group and Mad treatment (3.5 mg/kg) group (Mad). After treatment with Mad for seven days, the levels of LDH and CK-MB in serum were detected, H&E staining and TUNEL staining were performed. In vitro, 1.0 μm Mad was used for the subsequently experiment, observing cell apoptosis from Flow cytometry. Caspase-3 and AMD1 were detected in Western blotting. Flow cytometry and Western blotting were also performed after use of siRNA-AMD1-1. Then, analysis AMD1 potential function in cardiotoxicity from bioinformatics techniques including GO, KEGG, PPI, immune infiltration and molecular docking.
resultMaduramicin has myocardial toxic effects in vivo and vitro, which with AMD1 raised. When AMD1 was knocked down, toxic effects of Mad were alleviated. Apoptosis, proliferation and inflammation were the major pathophysiological changes in myocardial apoptosis process with AMD1-knockdown. This process involved in IL1A, IL1B, PTGS2, VEGFA, VEGFC and HBEFG, as hub genes related AMD1 cardiotoxicity function for Maduramicin. AMD1 was knocked down, their microenvironment changes: Effector memory CD4 T cell and Natural killer cell were more infiltrated, and Mast cell were less infiltrated.
conclusionMad exerted cardiotoxic effects by upregulating the AMD1 gene, which may be associated with cell apoptosis, proliferation and inflammatory response. AMD1 also had cardiotoxicity function, by the impact of both myocardial cells and the microenvironment they live.
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.