Evidence map›Paper›PMID 42071218›Full record

ArticleCell & bioscience2026

Cadmium impairs heart ventricular formation and disrupts polysialylated-NCAM/FGF receptor signaling in Xenopus tadpoles.

Pélagie Douchez, Ingrid Fliniaux, Yoshiko Takeda-Uchimura, Alain Martoriati, Matthieu Marin, Anne Harduin-Lepers, Katia Cailliau

Abstract read
In one paragraph

Article in Cell & bioscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Pélagie DouchezUniv. Lille, CNRS, UMR 8576-UGSF-Unité de Glycobiologie Structurale et Fonctionnelle, F-59000, Lille, France.
Ingrid FliniauxUniv. Lille, CNRS, UMR 8576-UGSF-Unité de Glycobiologie Structurale et Fonctionnelle, F-59000, Lille, France.
Yoshiko Takeda-UchimuraUniv. Lille, CNRS, UMR 8576-UGSF-Unité de Glycobiologie Structurale et Fonctionnelle, F-59000, Lille, France.
Alain MartoriatiUniv. Lille, CNRS, UMR 8576-UGSF-Unité de Glycobiologie Structurale et Fonctionnelle, F-59000, Lille, France.
Matthieu MarinUniv. Lille, CNRS, UMR 8576-UGSF-Unité de Glycobiologie Structurale et Fonctionnelle, F-59000, Lille, France.
Anne Harduin-LepersUniv. Lille, CNRS, UMR 8576-UGSF-Unité de Glycobiologie Structurale et Fonctionnelle, F-59000, Lille, France.
Katia CailliauUniv. Lille, CNRS, UMR 8576-UGSF-Unité de Glycobiologie Structurale et Fonctionnelle, F-59000, Lille, France. katia.maggio@univ-lille.fr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundExposure to cadmium, a trace metallic element, is a major health concern. Cadmium is associated with a higher risk and predisposition to cardiovascular disease. Identifying molecular targets involved in such an effect is complexified by in utero embryonic and fetal development.

methodsTo overcome those difficulties, we used the established vertebrate heart model of Xenopus laevis to analyze the neural cell adhesion molecules NCAM and FGF receptors involved in early cardiac development under cadmium treatment. Cadmium exposure is performed from fertilization until the completion of mature heart development at the end of stage 45. Additional molecular modifications occurring within the heart are detected in the expressing signaling system of Xenopus oocytes.

resultsExposure to cadmium results in the absence of heart ventricular myocardial trabeculae and disrupts the regulation of NCAM adhesion molecules and FGF receptor signaling in Xenopus. An increase in polysialylation (PSA) of NCAM is observed, accompanied by the deregulation in the expression of Golgi effectors Rab11 GTPase and Golph3. The sialyltransferases ST8Sia2 and ST8Sia4 are not increased at the transcriptional level but are accumulated in the Golgi apparatus. The highly sialylated NCAM interacts with the FGF receptor, prevents the formation of a complex with Integrin, FAK is O-GlcNAcylated, and the receptor translocation to the nucleus is impaired. Furthermore, the polysialylated-NCAM/FGF receptor signaling recruits higher amounts of Shp2 and leads to Erk2 hyperphosphorylation. Additionally, blocking FAK with a specific antibody in the normal polysialylated-NCAM/FGF receptor signaling causes the deregulated molecular phenotype.

conclusionsThese results represent a significant advancement for future studies in environmental toxicology and cardiac developmental dysfunctions resulting from cadmium exposure.

Indexed as

CadmiumFAKFGF receptorsGolgi apparatusHeartNCAMO-GlcNAcylationPolysialic acidXenopus

Identifiers

PMID42071218
PMCPMC13289098

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.