ReviewAmerican journal of physiology. Heart and circulatory physiology2015
Drug-induced mitochondrial dysfunction and cardiotoxicity.
Review in American journal of physiology. Heart and circulatory physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 266 papers, 5 of them syntheses 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
266 citing papers in PubMed, 5 syntheses or guidelines pooled it, 513 citations in OpenAlex.
- Pooled it
- Cardiotoxicity of HER2-Targeted Drugs When Combined with Other Drugs: A Systematic and Meta-analysis of Randomized Controlled Trials.Cardiovascular toxicology · 2024Pooled it
- Subcellular Effectors of Cocaine Cardiotoxicity: All Roads Lead to Mitochondria-A Systematic Review of the Literature.International journal of molecular sciences · 2023Pooled it
- The Role of Mitochondrial DNA Variation in Drug Response: A Systematic Review.Frontiers in genetics · 2021Pooled it
- Synthetic Cannabinoids and Cathinones Cardiotoxicity: Facts and Perspectives.Current neuropharmacology · 2021Pooled it
- XY0206 targets FLT3-dependent resistance states in acute myeloid leukemia.The Journal of clinical investigation · 2026Trial
- Circular RNAs in Drug-Induced Cardiotoxicity: Roles, Mechanisms, and Therapeutic Potential.Journal of biochemical and molecular toxicology · 2026Review
- Feasibility and Safety of Venetoclax for Cytoreduction During Induction Therapy in Newly Diagnosed Acute Promyelocytic Leukemia.European journal of haematology · 2026Article
- Review of in vitro approaches for assessing the toxicity of chemical stressors across diverse physiological systems.Toxicological sciences : an official journal of the Society of Toxicology · 2026Review
- Therapeutic Ultrasound in Cardiovascular Medicine: Applications of Low-intensity Pulsed Ultrasound and Ultrasound-targeted Microbubble Destruction.Cardiovascular drugs and therapy · 2026Review
- Embryotoxicity and Cardiotoxicity Assessment of Chemical Compounds Using Eggs of Lymnaea stagnalis.Current protocols · 2026Article
- Expanded Tox21 Biological Assay Panel for the Prediction of Drug-Induced Liver Injury and Cardiotoxicity.Environmental health perspectives · 2026Article
- Subthreshold Thermal Stress Aggravates Methamphetamine-Induced Cardiomyocyte Pyroptosis via the Mitochondrial ROS/BAX/mtDNA/NLRP3 Pathway.International journal of molecular sciences · 2026Article
- Targeting the Apelin-APJ Axis: A Promising Strategy to Mitigate Anthracycline-Induced Cardiotoxicity.Cardiovascular toxicology · 2026Review
- Resistance Exercise: A Potential Intervention for Managing Cardiovascular Health in Individuals with a History of Cancer.Sports medicine - open · 2026Article
- Ambrisentan attenuates cisplatin-related mitochondrial dysfunction in the heart via regulation of p53 and NF-κB signaling.Scientific reports · 2026Article
- Rational engineering of cholesterol-modified prodrug nanoassemblies for improving the tumor selectivity and safety of mitoxantrone.Fundamental research · 2026Article
- Doxorubicin-Induced Cardiac Remodeling: Mechanisms and Mitigation Strategies.Cardiovascular drugs and therapy · 2026Review
- Chemo-/radiotherapy-induced cardiomyopathy: roles of mitochondria and endoplasmic reticulum.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2026Review
- Mitochondrial Dysfunction: The Cellular Bridge from Emotional Stress to Disease Onset: A Narrative Review.Biomolecules · 2026Review
206 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
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Mitochondria has an essential role in myocardial tissue homeostasis; thus deterioration in mitochondrial function eventually leads to cardiomyocyte and endothelial cell death and consequent cardiovascular dysfunction. Several chemical compounds and drugs have been known to directly or indirectly modulate cardiac mitochondrial function, which can account both for the toxicological and pharmacological properties of these substances. In many cases, toxicity problems appear only in the presence of additional cardiovascular disease conditions or develop months/years following the exposure, making the diagnosis difficult. Cardiotoxic agents affecting mitochondria include several widely used anticancer drugs [anthracyclines (Doxorubicin/Adriamycin), cisplatin, trastuzumab (Herceptin), arsenic trioxide (Trisenox), mitoxantrone (Novantrone), imatinib (Gleevec), bevacizumab (Avastin), sunitinib (Sutent), and sorafenib (Nevaxar)], antiviral compound azidothymidine (AZT, Zidovudine) and several oral antidiabetics [e.g., rosiglitazone (Avandia)]. Illicit drugs such as alcohol, cocaine, methamphetamine, ecstasy, and synthetic cannabinoids (spice, K2) may also induce mitochondria-related cardiotoxicity. Mitochondrial toxicity develops due to various mechanisms involving interference with the mitochondrial respiratory chain (e.g., uncoupling) or inhibition of the important mitochondrial enzymes (oxidative phosphorylation, Szent-Györgyi-Krebs cycle, mitochondrial DNA replication, ADP/ATP translocator). The final phase of mitochondrial dysfunction induces loss of mitochondrial membrane potential and an increase in mitochondrial oxidative/nitrative stress, eventually culminating into cell death. This review aims to discuss the mechanisms of mitochondrion-mediated cardiotoxicity of commonly used drugs and some potential cardioprotective strategies to prevent these toxicities.
Indexed as
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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.