Evidence mapPaperPMID 41384295Full record

ReviewMolecular medicine reports2026

Deciphering epigenetic regulation in cardiac developmental toxicity: Mechanisms and implications (Review).

Ziling Qin, Ranran Chen, Dianrong Song

Abstract readReview
In one paragraph

Review in Molecular medicine 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.

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

3 authors.

Ziling Qin *Graduate School, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, P.R. China.
Ranran Chen *Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin 300250, P.R. China.
Dianrong SongDepartment of Obstetrics and Gynecology, The Second Affiliated Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin 300250, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As the first functional organ to form during vertebrate embryogenesis, the heart exhibits heightened susceptibility to developmental toxicity. Epigenetic regulatory mechanisms, including DNA methylation, histone modifications, non‑coding RNAs, N6‑methyladenosine methylation and chromatin accessibility alterations, mediate cardiac developmental toxicity induced by exogenous compounds including environmental chemicals and pharmaceuticals. The present review comprehensively summarizes the current understanding of the molecular mechanisms through which these compounds exert cardiac developmental toxicity through epigenetic regulation. An in‑depth analysis of research progress and technical challenges across diverse epigenetic pathways is provided. By summarizing recent evidence, the present review proposes candidate epigenetic biomarkers for cardiac developmental toxicity monitoring and explores potential intervention strategies targeting these pathways. Future research should prioritize multi‑omics integration technologies and clinical translation system development. These advances are anticipated to foster innovation in both mechanistic research and preventive strategy development for cardiac developmental toxicity.

Indexed as

CardiotoxicityEpigenesis, GeneticGene Expression Regulation, DevelopmentalHeartAnimalsDNA MethylationHistonesHumansHistonescardiac developmental toxicitychromatin accessibilityDNA methylationepigeneticshistone modificationsm6A methylationnon‑coding RNAs

Identifiers

PMID41384295
PMCPMC12728498

What Socratic 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 Socratic graph.