ArticleJournal of traditional and complementary medicine2025
Tectorigenin attenuates myocardial damage by doxorubicin-induced ferroptosis by activating the p62-Keap1-Nrf2/HO-1/GPX4 axis.
Article in Journal of traditional and complementary medicine, 2025. 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.
- Tectorigenin alleviates HFpEF by targeting the EGFR-EGR2-Acot1 axis to improve myocardial lipid metabolism.Acta pharmacologica Sinica · 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
Background: Anticancer agent doxorubicin is essential for cancer treatment but often causes cardiotoxicity. Tectorigenin has shown potential cardioprotective effects, but underlying mechanisms remain unclear. We aimed to investigate whether Tectorigenin attenuates doxorubicin-induced myocardial injury. Methods: Doxorubicin (DOX) was utilized in C57BL/6J mice and cardiomyocytes H9c2, to establish Results: DOX induced ferroptosis in H9c2 cells concentration-dependently and time-dependently, which was alleviated by Tectorigenin treatment. ML385 or K67 abolished Tectorigenin's inhibition on DOX-induced H9c2 cell ferroptosis. Mechanistically, Tectorigenin promoted the expressions of p62 and p-p62, leading to decreased Keap1 expression. This cascade facilitated Nrf2 nuclear translocation and subsequently elevated HO-1 and GPX4 expressions. Moreover, Tectorigenin treatment improved cardiac function, myocardial injury, fibrosis and mitochondrial function in C57BL/6J mice induced by DOX, as well as ferroptosis. Conclusion: Our findings reveal that Tectorigenin attenuates DOX-induced ferroptosis and myocardial damage by activating the p62-Keap1-Nrf2/HO-1/GPX4 axis, this may provide a therapeutic strategy for mitigating cardiotoxicity associated with chemotherapeutic agents.
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.