ArticleWorld journal of cardiology2025
Mechanism of myocardial damage induced by doxorubicin
Article in World journal of cardiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed.
- Impact of CaInternational journal of molecular sciences · 2026Review
- Mechanisms and the Role of p38 MAPK Signaling in Doxorubicin-Induced Cardiotoxicity: A Review.International journal of general medicine · 2026Review
- Walras modulates sex-dependent endoplasmic reticulum stress in cardiomyopathy.Frontiers in physiology · 2026Article
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
backgroundThe clinical application of doxorubicin (DOX) is limited by its potential to cause cardiac cardiotoxicity.
aimTo investigate the correlation between calumenin (CALU) and mitochondrial kinetic-related proteins in rats with DOX cardiomyopathy.
methodsA rat model of DOX-induced cardiomyopathy was used to evaluate the effects of DOX. We observed the effect of DOX on electrical conduction in cardiomyocytes using the electromapping technique. Masson staining was performed to evaluate myocardium fibrosis. Electron microscopy was used to observe the changes in pathological ultrastructure of the myocardium. Western blotting and ELISAs were performed to detect protein levels and intracellular free Ca
resultsDOX slowed conduction and increased conduction dispersion in cardiomyocytes. The myocardial pathology in rats treated with DOX exhibited a significant deterioration, as demonstrated by an increase in mitochondrial Ca
conclusionIncreased cytoplasmic free calcium ion concentration induces calcium overload in ventricular myocytes, leading to decreased Cx43 protein, slowed conduction in myocytes, and increased conduction dispersion, resulting in arrhythmias.
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.