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Open research questions in Chemotherapy-induced cardiotoxicity and mitigation

388 gap statements mined from Chemotherapy-induced cardiotoxicity and mitigation papers in our 7.9M-paper local library, which holds 1,465 papers on the topic — drawn mostly from each paper's own stated research gap, future-work, challenge and limitation notes, and its abstract. The ones listed below are a selection still marked open; each names the study that raised it, with a DOI link where the paper has one.

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What the literature leaves open

  • One challenge in this study was the potential for selection bias, as the control group was not matched to the study cohort. Another challenge was the limited sample size, which may have affected the generalizability of the results. The study also faced challenges in terms of data quality and availability, as some patients had missing or incomplete data.

    Ventricular Arterial Coupling as a Marker of Early Cardiotoxicity in Survivors of Childhood Cancer · 2026 · DOI

  • There is limited data studying ventriculoarterial coupling in pediatric patients, particularly in the context of childhood cancer survivors. Prior studies have focused on adult populations or other patient groups, leaving a gap in the understanding of cardiotoxicity in childhood cancer survivors.

    Ventricular Arterial Coupling as a Marker of Early Cardiotoxicity in Survivors of Childhood Cancer · 2026 · DOI

  • External validation of the findings is required. Further studies should investigate the use of dedicated cardiac protocols for PET/CT imaging. Research on the optimal preparation and interpretation of myocardial FDG uptake is needed.

    Predictive value of left ventricular 18F-FDG PET/CT derived parameters and uptake patterns for chemotherapy-induced cardiotoxicity in patients with lymphoma · 2026 · DOI

  • One challenge is the need for individualized cardiovascular risk assessment and cardioprotective interventions. Another challenge is the need for close surveillance and multidisciplinary collaboration. The paper also notes the challenge of managing cardiotoxicity in patients with cancer, particularly in those with preexisting cardiovascular comorbidities.

    Permissive Cardiotoxicity: An Evolving Paradigm · 2026 · DOI

  • There is a need for recognition and confidence in managing cardiotoxicity among general cardiologists and oncologists. The growing population of patients with cancer requires effective management of cardiotoxicity. There is a lack of clear guidelines for the management of permissive cardiotoxicity.

    Permissive Cardiotoxicity: An Evolving Paradigm · 2026 · DOI

  • The need to develop effective therapeutic strategies to ameliorate cardiac injury.

    Metabolic reprogramming of CCR2+ MHC IIhigh macrophage contributes to myocarditis induced by Doxorubicin · 2026 · DOI

  • The paper identifies a research gap in the lack of systematic examination of studies applying ML models to predict a broad range of drug-induced cardiotoxicity outcomes. Prior research has largely focused on specific mechanisms, leaving a gap in the understanding of ML models for predicting diverse cardiotoxic outcomes.

    Machine Learning for Predicting Human Drug-Induced Cardiotoxicity: A Scoping Review · 2025 · DOI

  • There is a need for effective preventive strategies to mitigate anthracycline-related cardiotoxicity. The long-term cardiovascular consequences of anthracycline exposure are a growing concern. Current cardioprotective measures may not be sufficient to prevent anthracycline-induced cardiotoxicity.

    Lifestyle and Pharmacological Interventions to Prevent Anthracycline-Related Cardiotoxicity in Cancer Patients · 2025 · DOI

  • Limited oncology-specific protocols for cancer therapy-induced hypertension. Need for targeted guidelines and improved long-term care for affected patients. Lack of understanding of the relationship between hypertension and cancer treatment.

    Navigating the Complexities of Cancer Treatment-Induced Hypertension · 2025 · DOI

  • There are conflicting results regarding symptom severity and prognosis among those with and without TTNtv mutation.

    Titin-Truncating Variants as Genetic Determinants of Chemotherapy-Induced Cardiomyopathy: A Review · 2026 · DOI

  • Left ventricular ejection fraction (LVEF) is insensitive to subclinical myocardial injury, and locally validated thresholds for global longitudinal strain (GLS) are lacking in Vietnamese patients.

    Frequency and Risk Factors of Cancer Therapy-Related Cardiac Dysfunction in Patients Receiving Chemotherapy: A Prospective Cohort Study at a Tertiary Centre: doi: 10.7417/CT.2026.2157 · 2026

  • To date, large-scale prospective data on cardiac imaging after ICI are still lacking.

    Multimodality imaging for the detection of cardiotoxicity in cancer patients treated with immune checkpoint inhibitors · 2026 · DOI

  • Given the rarity of myeloid malignancies and the multifactorial etiology of CVD, together with the epidemiologic evidence presented in this study, further etiologic investigations followed by interventional research are warranted to inform the design of optimal integrative care strategies for patients with myeloid neoplasms.

    Myeloid Neoplasms Meet Cardiovascular Epidemiology: A Call for Integrated Cardio-hematology Care · 2026 · DOI

  • Longitudinal trajectories of N-terminal pro-B-type natriuretic peptide (NT-proBNP), a biomarker of myocardial stress, remain insufficiently characterized.

    Longitudinal changes in NT-proBNP after breast cancer radiotherapy: clinical determinants of its trajectory and association with cardiac dysfunction (BACCARAT study) · 2026 · DOI

  • However, whether PTN exerts protective effects against DOX-induced cardiotoxicity (DIC) remains unclear.

    Cardiac PTN-SIRT1 axis alleviates oxidative stress and promotes mitochondrial energy reprogramming to mitigate doxorubicin-induced cardiotoxicity through AMPK/PGC1α signaling · 2026 · DOI

  • Nerve injury-induced protein 1 (NINJ1), a regulator of inflammation and cell death, has not been explored in this context.

    NINJ1 Aggravates Doxorubicin-Induced Cardiotoxicity by Suppressing AMPK-Mediated HIF-1α Deubiquitination · 2026 · DOI

  • Although NAD+ deficiency has been implicated in cardiovascular pathology, its role in DOX-induced cardiotoxicity (DIC) remains poorly understood.

    FOXO1-NMNAT3 axis dysregulation promotes doxorubicin cardiotoxicity: NAD + replenishment as a redox-targeted antioxidant therapy · 2025 · DOI

  • Although extensive research has focused on Dox-induced cardiotoxicity (DIC), its mechanism remains elusive.

    ALOX15 Modulates Ferroptosis via the Reactive Oxygen Species-Mediated MAPK Pathway in Doxorubicin-Induced Cardiotoxicity · 2025 · DOI

  • However, the underlying mechanisms remain unclear, and whether mitochondrial short open reading frame-encoded peptides can mitigate DOX-induced cardiotoxicity is unknown.

    Mitochondrial sORF-Encoded Peptide MODICA Protects the Heart From Doxorubicin-Induced Cardiac Injury by Suppressing VDAC Oligomerization · 2025 · DOI

  • Cardio-oncology is an emerging interdisciplinary field dedicated to the early detection and treatment of adverse cardiovascular events associated with anticancer treatment, and current clinical management of anticancer-treatment-related cardiovascular toxicity (CTR-CVT) remains limited by a lack of detailed phenotypic data.

    Precision Cardio-oncology: Update on Omics-Based Diagnostic Methods · 2024 · DOI

  • However, its potential protective effects against Dox-induced cardiotoxicity (DIC) remain unexplored.

    Cardioprotective effect of Saussurea involucrata injection against Doxorubicin-induced cardiotoxicity by network pharmacology analysis and experimental verification · 2024 · DOI

  • The study was a retrospective observational study. The discriminatory performance of PET-derived parameters was moderate. Myocardial FDG uptake is strongly influenced by substrate availability and patient preparation. The study lacked dedicated cardiac protocols for PET/CT imaging.

    Predictive value of left ventricular 18F-FDG PET/CT derived parameters and uptake patterns for chemotherapy-induced cardiotoxicity in patients with lymphoma · 2026 · DOI

  • Investigating the effects of macrophage PKM2 inhibition on DOX-conditioned cardiomyocytes in vivo, - Exploring the therapeutic potential of using Shikonin to inhibit PKM2 to ameliorate cardiac injury, - Further investigating the role of PKM2 in CCR2+ macrophage metabolic…

    Metabolic reprogramming of CCR2+ MHC IIhigh macrophage contributes to myocarditis induced by Doxorubicin · 2026 · DOI

  • Ongoing research is needed to develop targeted guidelines for cancer therapy-induced HTN, - Research is needed to improve the long-term care of cancer patients affected by treatment-induced HTN, - Investigations into the chronic effects of platinum-based therapies on blood pressure…

    Navigating the Complexities of Cancer Treatment-Induced Hypertension · 2025 · DOI

  • Despite its efficacy, Dox induces numerous adverse effects in humans with significant cardiotoxicity, posing a major limitation to its use.

    Cardioprotective effect of Saussurea involucrata injection against Doxorubicin-induced cardiotoxicity by network pharmacology analysis and experimental verification · 2024 · DOI

Most-cited papers in Chemotherapy-induced cardiotoxicity and mitigation

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Open questions raised by papers listed on this page include: (1) There is limited data studying ventriculoarterial coupling in pediatric patients, particularly in the context of childhood cancer survivors (“Ventricular Arterial Coupling as a Marker of Early Cardiotoxicity in Survivors…”, 2026); (2) Further studies should investigate the use of dedicated cardiac protocols for PET/CT imaging (“Predictive value of left ventricular 18F-FDG PET/CT derived parameters and…”, 2026); (3) There is a need for recognition and confidence in managing cardiotoxicity among general cardiologists and oncologists (“Permissive Cardiotoxicity: An Evolving Paradigm”, 2026); (4) To date, large-scale prospective data on cardiac imaging after ICI are still lacking (“Multimodality imaging for the detection of cardiotoxicity in cancer patients…”, 2026); (5) Longitudinal trajectories of N-terminal pro-B-type natriuretic peptide (NT-proBNP), a biomarker of myocardial stress, remain insufficiently characterized (“Longitudinal changes in NT-proBNP after breast cancer radiotherapy: clinical…”, 2026). 388 gap statements have been mined from Chemotherapy-induced cardiotoxicity and mitigation papers in our 7.9M-paper local library, which holds 1,465 papers on the topic; the gaps come from whichever of those papers state one. They are mostly the research gaps the authors state and the papers' abstracts, plus future-work, limitations and challenges passages. The ones listed below are a selection still marked open; each names the study that raised it, with a DOI link where the paper has one, so you can read the original claim in context.

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