ArticleCardiovascular toxicology2026
Zebrafish Model Reveals Early Electrocardiographic and Molecular Signatures of Doxorubicin-Induced Cardiotoxicity.
Article in Cardiovascular toxicology, 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
8 authors.
Funding
Abstract
Doxorubicin (DOX) is a highly effective anthracycline widely used in cancer therapy but limited by its dose-dependent cardiotoxicity, which may result in arrhythmia, dilated cardiomyopathy, and heart failure. Conventional surveillance tools, including echocardiography and serum biomarkers, often identify injury only after substantial cardiac dysfunction has occurred. This underscores the need for early markers with mechanistic relevance. In this study, we developed an integrated zebrafish platform combining pathophysiological evaluation, electrocardiography (ECG), and transcriptomic profiling to establish a novel approach for early detection of DOX-induced cardiotoxicity (DIC). Consistent with human and mammalian models, DOX administration in adult zebrafish resulted in ventricular enlargement, myocardial fiber disarray, and elevated troponin I levels. ECG recordings revealed dose-dependent conduction disturbances, notably progressive PR interval and QRS prolongation, with P wave widening at higher doses. These findings identify the PR interval as a sensitive, early index of conduction impairment in the zebrafish DIC model, consistent with clinical reports linking PR prolongation to adverse outcomes. RNA sequencing further identified transcriptional pathways associated with conduction delay, with dysregulation of sodium channels (scn5lab, scn1lab), gap junction proteins (cx43, cx40.8), and transcriptional regulators (nkx2.5, tbx family). Notably, scn1lab expression declined progressively, cx43 and nkx2.5 were upregulated, showing temporal changes that co-occurred with the observed ECG and structural phenotypes. Together, these results support adult zebrafish as a scalable platform for cardiotoxicity screening and highlight PR interval prolongation as an early electrophysiological marker of DOX-associated conduction disturbance. The transcriptomic signatures are presented as correlative, hypothesis-generating candidates relevant to cardiac conduction and remodeling.
Indexed as
Identifiers
What Socratic 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 Socratic graph.