ArticleiScience2024
AMPD3 promotes doxorubicin-induced cardiomyopathy through HSP90α-mediated ferroptosis.
Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 5 papers.
What it found
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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.
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Who cites it
5 citing papers in PubMed.
- Regulation of HSP90AA1/NRF2 by BDNF Contributes to the Attenuation of Rotenone-Induced Oxidative Stress in Parkinson's Disease Models.Molecular neurobiology · 2026Article
- Engineered Sulfonated Bacterial Cellulose Hydrogel with Dual Bioactive-Drug Delivery Functions for Precision Treatment of Psoriasis.Biomacromolecules · 2025Article
- Review
- Doxorubicin-Induced Cardiotoxicity: A Comprehensive Update.Journal of cardiovascular development and disease · 2025Review
- Tea Polyphenols Mitigate Radiation-Induced Ferroptosis and Intestinal Injury by Targeting the Nrf2/HO-1/GPX4 Signaling Pathway.Antioxidants (Basel, Switzerland) · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Doxorubicin (DOX), a widely used anticancer drug, can induce myocardial damage, and current treatments are limited. Our research identified AMPD3 upregulation in DOX-induced cardiotoxicity (DIC), and we hypothesized that AMPD3 may contribute to cardiac injury by regulating mitochondrial dynamics and ferroptosis. We generated AMPD3 knockout (KO) mice and AC16 cell models with AMPD3 knockdown/overexpression, using various methods to explore underlying mechanisms. AMPD3 KO mice showed improved ejection fractions and reduced myocardial injury compared to controls. Transcriptome sequencing revealed reduced HSP90AA1, HSP90B1, ACSL4, and dynamin-related protein 1 (DRP1) levels. We further demonstrated that AMPD3 interacts with HSP90α, activating DRP1, leading to mitochondrial fission, increased reactive oxygen species (ROS) release, and ACSL4-mediated ferroptosis. Our findings suggest inhibiting AMPD3 during DOX treatment may alleviate myocardial damage, highlighting mitochondrial function and ferroptosis as potential therapeutic targets for DIC.
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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.