ReviewCellular and molecular life sciences : CMLS2022
Anthracycline-induced cardiotoxicity and cell senescence: new therapeutic option?
Review in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Effects of Physical Activity on Cardiotoxicity and Cardio respiratory Function in Cancer Survivors Undergoing Chemotherapy: A Systematic Review and Meta-Analysis.Integrative cancer therapiesPooled it
- Cardiovascular ageing: hallmarks, signaling pathways, diseases and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Therapy-induced senescence in breast cancer and cardiovascular disease: a double-edged biological process.Frontiers in cardiovascular medicine · 2026Review
- Efficacy evaluation of Wenxin Keli in treating anthracycline-induced atrial arrhythmias (WARMA study): protocol for a multicenter, randomized, double-blind, placebo-controlled clinical trial.Frontiers in cardiovascular medicine · 2026Article
- IER3 drives the transition from sepsis-associated AKI to CKD by suppressing the mitochondrial translocation of PRDX5.Cellular and molecular life sciences : CMLS · 2025Article
- An mTOR-Tfeb-Fabp7a Axis Ameliorates bag3 Cardiomyopathy via Decelerating Cardiac Aging.Aging cell · 2025Article
- Reversing coma by senolytics and stem cells: the future is now.Journal of translational medicine · 2025Review
- EBBP-Mediated Integrated Stress Response Attenuates Anthracycline-Induced Cardiotoxicity by Inhibiting the Ferroptosis of Cardiomyocytes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Multidisciplinary strategies to reduce radiotherapy-induced cardiotoxicity in breast cancer: surgical and technological innovations.Frontiers in oncology · 2025Review
- Pleiotropic Multi-Drug Co-Assembled Nanocomposites Offer Protection Against Doxorubicin-Induced Cardiotoxicity.International journal of nanomedicine · 2025Article
- Review
- Metrnl: a promising biomarker and therapeutic target for cardiovascular and metabolic diseases.Cell communication and signaling : CCS · 2024Review
- Primary Protection of Diosmin Against Doxorubicin Cardiotoxicity via Inhibiting Oxido-Inflammatory Stress and Apoptosis in Rats.Cell biochemistry and biophysics · 2024Article
- Article
- Therapy-induced senescence is finally escapable, what is next?Cell cycle (Georgetown, Tex.) · 2024Review
- Recent Advances in the Mechanisms of Cell Death and Dysfunction in Doxorubicin Cardiotoxicity.Reviews in cardiovascular medicine · 2023Review
- Identification and functional analysis of senescent cells in the cardiovascular system using omics approaches.American journal of physiology. Heart and circulatory physiology · 2023Review
- Pregnenolone Inhibits Doxorubicin-Induced Cardiac Oxidative Stress, Inflammation, and Apoptosis-Role of Matrix Metalloproteinase 2 and NADPH Oxidase 1.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Coronary atherosclerosis and chemotherapy: From bench to bedside.Frontiers in cardiovascular medicine · 2023Review
- Assessment of Cardiovascular Function in Childhood Leukemia Survivors: The Role of the Right Heart.Children (Basel, Switzerland) · 2022Article
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 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anthracyclines are chemotherapeutic drugs widely used in the frontline of cancer treatment. The therapeutic mechanisms involve the stabilization of topoisomerase IIα, DNA, and the anthracycline molecule in a ternary complex that is recognized as DNA damage. Redox imbalance is another vital source of oxidative DNA damage. Together, these mechanisms lead to cytotoxic effects in neoplastic cells. However, anthracycline treatment can elicit cardiotoxicity and heart failure despite the therapeutic benefits. Topoisomerase IIβ and oxidative damage in cardiac cells have been the most reported pathophysiological mechanisms. Alternatively, cardiac cells can undergo stress-induced senescence when exposed to anthracyclines, a state primarily characterized by cell cycle arrest, organelle dysfunction, and a shift to senescence-associated secretory phenotype (SASP). The SASP can propagate senescence to neighboring cells in an ongoing process that leads to the accumulation of senescent cells, promoting cellular dysfunction and extracellular matrix remodeling. Therefore, the accumulation of senescent cardiac cells is an emerging pathophysiological mechanism associated with anthracycline-induced cardiotoxicity. This paradigm also raises the potential for therapeutic approaches to clear senescent cells in treating anthracycline-induced cardiotoxicity (i,e, senolytic therapies).
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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.