ArticleBiomedical reports2025
Metabolomic profiling reveals amino acid dysregulation in congenital heart disease: Arginine-induced embryonic malformations and pathogenic insights.
Article in Biomedical reports, 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Congenital heart disease (CHD) is the most common form of malformation seen in China. In most cases, its pathogenesis is unclear. The present study aimed to identify the differential metabolites and novel screening markers to discover the potential pathogenesis of CHD. Cultured amniotic fluid cells from pregnant patients carrying CHD-affected (n=24) or healthy (n=24) fetuses were collected. Untargeted metabolomics was performed on the cells. A total of 292 metabolites (172 up- and 120 downregulated) were significantly different between the CHD and control groups (variable importance on projection >1 and P<0.05). Significantly different metabolites were screened and analyzed using hierarchical clustering and Kyoto Encyclopedia of Genes and Genomes metabolic pathway enrichment. These data demonstrated that amino acid metabolism was considerable elevated. The most notable differential metabolites were lysine and arginine, suggesting they may play an important role in heart development. When arginine were used to treat pregnant mice, embryos (embryonic day 15.5) demonstrated increased malformation rate, the litter size decreased (4.3±1.03 vs. 6.5±1.05, P<0.01) and the naked deformity rate significantly increased (30.8 vs. 0.0%, P<0.001), compared with the controls. The embryonal heart cavity was larger and the heart wall became thinner. The present study suggested that amino acid metabolites may serve a crucial role in heart development and could serve as potential screening markers for CHD. Additionally, the adverse effects of arginine treatment on embryonic development highlight its role in CHD pathogenesis.
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.