ReviewCirculation research2020
Mitochondrial Determinants of Doxorubicin-Induced Cardiomyopathy.
Review in Circulation research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06881940 (Rationale and Design of a Cardiac Rehabilitation Program on the Prevention of Cardiotoxicity in Breast Cancer Patients Undergoing Treatment With Anthracyclines and/or Trastuzumab), which is not on this map. Cited by 327 papers, 1 of them a synthesis that pooled it.
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.
Rationale and Design of a Cardiac Rehabilitation Program on the Prevention of Cardiotoxicity in Breast Cancer Patients Undergoing Treatment With Anthracyclines and/or Trastuzumab: A Randomized, Active Control Group, Open-Label Trial
Who cites it
327 citing papers in PubMed, 1 synthesis or guideline pooled it, 542 citations in OpenAlex.
- Exercise for the mitigation of cancer therapy-related cardiac dysfunction in breast cancer patients treated with anthracyclines: a systematic review and meta-analysis.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2026Pooled it
- Doxorubicin-induced hepatotoxicity: a multifaceted pathogenesis from mitochondrial collapse to immune remodeling and epigenetic memory.Archives of toxicology · 2026Review
- Mitochondrial superoxide-induced mitohormesis is mediated by citrate and cardioprotective.Science advances · 2026Article
- Nutritional Prevention of Oxidative Stress-Induced Cardiotoxicity in Pediatric Cardio-Oncology: Molecular Mechanisms and Translational Perspectives-A Narrative Review.International journal of molecular sciences · 2026Review
- Early cardiac proteomic profiling in a long-latency doxorubicin cardiomyopathy model exhibits sexual dimorphism for cardioprotection.Journal of molecular and cellular cardiology plus · 2026Article
- From aging biology to cardiac biotechnology: emerging platforms for modeling cardiac aging.JCI insight · 2026Review
- Exploring the role of CaMKII in exercise-induced cardioprotection.Human cell · 2026Review
- Sotagliflozin ameliorates doxorubicin-induced cardiomyopathy by regulating inflammation and mitochondrial dysfunction through the AMPK/mTOR pathway.Experimental and therapeutic medicine · 2026Article
- Molecular mechanisms of iron metabolism and ferroptosis in cardiovascular diseases and intervention strategies targeting natural products (Review).Molecular medicine reports · 2026Review
- ATP Synthase Inhibitory Factor-1 Deficiency Attenuates Doxorubicin Cardiotoxicity by Preserving Mitochondrial Structure and Function.International journal of molecular sciences · 2026Article
- Natural-Origin Compounds as Future Precision Partners in Combination Cancer Therapy.Medicina (Kaunas, Lithuania) · 2026Review
- Dose-Dependent Genome-Wide DNA Methylation Remodeling by Metformin Modulates Doxorubicin Sensitivity in Cardiac Cells.Epigenomes · 2026Article
- The mitochondrial protease, LonP1, is a potential cardioprotective target for attenuating doxorubicin-induced cardiomyocyte death.Journal of translational medicine · 2026Article
- Rewiring NADH Metabolism Through NQO1-Mediated Redox Cycling for Targeted Follicular Lymphoma Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Review
- Endothelial progenitor cell susceptibility to DNA damaging and DDR-modulating compounds determines endothelial differentiation accuracy.Stem cell research & therapy · 2026Article
- Impact of CaInternational journal of molecular sciences · 2026Review
- Trajectory and Determinants of Left Ventricular Dysfunction Following Anthracycline-Based Therapy Among Breast Cancer Patients: A Three-Year Cohort Analysis in Indonesia.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Mitochondrial protein COXFA4L3 (C15ORF48) confers resistance to DNA-damaging anticancer agents by repressing mitochondrial DNA damage responses.Scientific reports · 2026Article
- Peroxiredoxin Ⅲ safeguards cardiac function against doxorubicin by regulating mitochondrial quality control via HRedox biology · 2026Article
267 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Anthracycline-based chemotherapy can result in the development of a cumulative and progressively developing cardiomyopathy. Doxorubicin is one of the most highly prescribed anthracyclines in the United States due to its broad spectrum of therapeutic efficacy. Interference with different mitochondrial processes is chief among the molecular and cellular determinants of doxorubicin cardiotoxicity, contributing to the development of cardiomyopathy. The present review provides the basis for the involvement of mitochondrial toxicity in the different functional hallmarks of anthracycline toxicity. Our objective is to understand the molecular determinants of a progressive deterioration of functional integrity of mitochondria that establishes a historic record of past drug treatments (mitochondrial memory) and renders the cancer patient susceptible to subsequent regimens of drug therapy. We focus on the involvement of doxorubicin-induced mitochondrial oxidative stress, disruption of mitochondrial oxidative phosphorylation, and permeability transition, contributing to altered metabolic and redox circuits in cardiac cells, ultimately culminating in disturbances of autophagy/mitophagy fluxes and increased apoptosis. We also suggest some possible pharmacological and nonpharmacological interventions that can reduce mitochondrial damage. Understanding the key role of mitochondria in doxorubicin-induced cardiomyopathy is essential to reduce the barriers that so dramatically limit the clinical success of this essential anticancer chemotherapy.
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.