ArticleHuman cell2026
Herbacetin alleviates acute doxorubicin cardiotoxicity via regulating the ERK1/2-FOXO3a signaling pathway.
Article in Human cell, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Targeting FOXO3 for the Management of Heart Failure: Current Evidence and Future Directions.Pharmaceuticals (Basel, Switzerland) · 2026Review
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
Abstract
Doxorubicin (DOX) is a commonly prescribed chemotherapeutic regimen, but its practice is challenged by cardiotoxicity risks. Herbacetin (HBT), a bioactive flavonoid compound, has demonstrated anti-oxidative, anti-inflammation, and anti-tumor properties. This study aimed to evaluate the protective effects of HBT against DOX cardiotoxicity along with the underlying mechanisms. In vitro, HBT enhanced cell survival, prevented DNA damage, reduced mitochondrial ROS, and maintained mitochondrial integrity in DOX-treated cardiomyocytes. Using an acute DOX cardiotoxicity rat model, HBT prevented DOX-induced declined cardiac function and reversed cardiac remodeling depicted by increased cell size. RNA sequence analysis of PBS-, DOX-, and DOX + HBT-treated H9c2 cardiomyocytes suggested the involvement of the MAPK signaling pathway in cardioprotective effects of HBT. Specifically, the level of phosphorylated ERK1/2 was increased in DOX-treated cardiomyocytes, which declined in the presence of HBT. The decreased level of FOXO3a (downstream factor of ERK1/2) by DOX was further restored by HBT. Lastly, the knockdown of FOXO3a abrogated the cardioprotective benefits of HBT. Our data suggest that HBT mitigates acute DOX cardiotoxicity via regulating the ERK1/2-FOXO3a signaling pathway, highlighting its potential as a novel therapeutic agent against DOX cardiotoxicity.
Indexed as
Identifiers
41774278What 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.