ArticleFrontiers in oncology2022
Doxorubicin-induced cardiotoxicity is mediated by neutrophils through release of neutrophil elastase.
Article in Frontiers in oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed.
- Doxorubicin-Induced Cardiac Remodeling: Mechanisms and Mitigation Strategies.Cardiovascular drugs and therapy · 2026Review
- Doxorubicin induces bone loss and modifies multiple cell populationsJournal of bone oncology · 2026Article
- Emerging Targets and Treatments for Doxorubicin-Induced Cardiac Inflammation.Journal of inflammation research · 2026Review
- Integrating Microarray Analysis, Machine Learning, and Molecular Docking to Explore the Mechanism of Doxorubicin-induced Cardiotoxicity.Current medicinal chemistry · 2026Article
- Sarcoma: Cardiovascular and Oncologic Considerations: JACC: CardioOncology State-of-the-Art Review.JACC. CardioOncology · 2025Review
- Computation-aided design of rod-shaped nanoparticles for tumoral targeting.Journal of controlled release : official journal of the Controlled Release Society · 2025Article
- Multifaceted roles of neutrophils in cardiac disease.Journal of leukocyte biology · 2025Review
- Cardioprotection strategies for anthracycline cardiotoxicity.Basic research in cardiology · 2025Review
- Immuno-inflammatory mechanisms in cardio-oncology: new hopes for immunotargeted therapies.Frontiers in oncology · 2025Review
- Inflammation in Chemotherapy-Induced Cardiotoxicity.Current cardiology reports · 2024Review
- Cytotoxic T cells drive doxorubicin-induced cardiac fibrosis and systolic dysfunction.Nature cardiovascular research · 2024Article
- A longitudinal evaluation of oxidative stress - mitochondrial dysfunction - ferroptosis genes in anthracycline-induced cardiotoxicity.BMC cardiovascular disorders · 2024Article
- Pharmacological activation of GPX4 ameliorates doxorubicin-induced cardiomyopathy.Redox biology · 2024Article
- Neutrophil extracellular traps mediate cardiomyocyte ferroptosis via the Hippo-Yap pathway to exacerbate doxorubicin-induced cardiotoxicity.Cellular and molecular life sciences : CMLS · 2024Article
- B-Cell Immune Checkpoints Come of Age in Cardio-oncology.Circulation research · 2024Article
- Anticancer drugs and cardiotoxicity: the role of cardiomyocyte and non-cardiomyocyte cells.Frontiers in cardiovascular medicine · 2024Review
- Analysis and Validation of Critical Signatures and Immune Cell Infiltration Characteristics in Doxorubicin-Induced Cardiotoxicity by Integrating Bioinformatics and Machine Learning.Journal of inflammation research · 2024Article
- Circulating microRNAs and Cytokines as Prognostic Biomarkers for Doxorubicin-Induced Cardiac Injury and for Evaluating the Effectiveness of an Exercise Intervention.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Article
- RGS7 balances acetylation/de-acetylation of p65 to control chemotherapy-dependent cardiac inflammation.Cellular and molecular life sciences : CMLS · 2023Article
- CannabimimeticPharmaceutics · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanisms by which Doxorubicin (Dox) causes acute and late cardiotoxicity are not completely understood. One understudied area is the innate immune response, and in particular the role of neutrophils in Dox-induced cardiotoxicity. Here, using echocardiography, flow cytometry and immunofluorescence staining, we demonstrated increased infiltration of neutrophils that correlated with decreased heart function, disruption of vascular structures and increased collagen deposition in the heart after Dox treatment. Depleting neutrophils protected the heart from Dox-induced cardiotoxicity and changes in vascular structure. Furthermore, our data using neutrophil elastase (NE) knock-out mice and the NE inhibitor AZD9668 suggest that neutrophils cause this damage by releasing NE and that inhibiting NE can prevent Dox-induced cardiotoxicity. This work shows the role of neutrophils and NE in Doxorubicin-induced cardiotoxicity for the first time and suggests a new possible therapeutic intervention.
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.