Molecular Pathogenesis and Novel Therapeutic Targets in Oncologic Cardiotoxicity
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".
Deadline for manuscript submissions: 31 July 2026 | Viewed by 26
Special Issue Editor
Interests: heart failure; atrial fibrillation; cardiovascular medicine; cardiology; ultrasound; internal medicine; chronic heart failure; clinical practice
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
The increasing success of cancer therapies has brought to light the urgent need to understand and manage cancer therapy-related cardiotoxicity (CTRCD), a major cause of morbidity and mortality among cancer survivors. CTRCD is a heterogeneous phenomenon that manifests as myocardial dysfunction and may progress to heart failure (HF) with either reduced ejection fraction (HFrEF) or preserved ejection fraction (HFpEF).
This Special Issue of the International Journal of Molecular Sciences (IJMS) aims to provide a platform for cutting-edge research exploring the molecular, genetic, and cellular foundations of CTRCD. Building upon the distinct pathophysiology of HFrEF and HFpEF in this patient population (as highlighted in the foundational paper by Tana et al.), the goal is to deepen our understanding of altered signaling pathways as well as myocardial damage and repair mechanisms and to identify new pharmacological targets for cardioprotection.
We invite original research articles, short communications, and high-quality reviews focusing on the following molecular and translational areas:
- Distinct molecular mechanisms of cardiotoxicity:
- Anthracycline-induced damage (HFrEF): Specific roles of reactive oxygen species (ROS), mitochondrial dysfunction, and apoptotic pathways (e.g., p53, caspases) in irreversible cardiomyocyte injury.
- Targeted therapy (HFrEF/HFpEF): Disruption of survival pathways (e.g., HER2/ErbB2-PI3K/Akt-MAPK axis) by trastuzumab, and molecular mechanisms of endothelial and vascular alterations induced by specific tyrosine kinase inhibitors (TKIs) (e.g., VEGFR/PDGFR).
- Immunotherapies and inflammasomes: The role of cytokines, T-cell infiltration, and inflammatory mediators (e.g., NLRP3 inflammasome) in the pathogenesis of ICI-induced myocarditis.
- Molecular predictors and biomarkers:
- Novel molecular biomarkers: Identification and validation of circulating molecular markers (e.g., microRNAs, circulating DNA, exosomes) that reflect subclinical myocardial injury, fibrosis, or inflammation.
- Genomics and pharmacogenomics: Analysis of genetic variants (e.g., TOP2B polymorphisms, drug metabolism-related genes) predisposing patients to specific cardiotoxicity phenotypes.
- HFpEF molecular pathophysiology: Molecular mechanisms of ventricular stiffness, focusing on the extracellular matrix (ECM), TGF-\beta signaling, and the role of cardiac fibroblasts in cancer therapy-induced fibrosis
- Novel therapeutic targets and cardioprotective strategies:
- Mitochondrial cardioprotection: Development of agents that protect mitochondrial function or reduce oxidative stress in cardiomyocytes.
- Signaling pathway modulators: Agents that restore survival pathways or modulate the inflammatory response to mitigate cardiac injury.
- Emerging therapies: Mechanistic investigations into the cardioprotective, anti-inflammatory, and anti-fibrotic actions of drugs like SGLT2 inhibitors and ARNIs in the context of CTRCD.
- Molecular crosstalk in comorbidities:
- The molecular impact of comorbidities (e.g., diabetes, hypertension) on the susceptibility to cardiotoxicity (e.g., role of adipokines, insulin resistance) and the etiology of HFpEF in cancer patients.
The ultimate goal is to advance molecular understanding to support the development of personalized diagnostic and therapeutic approaches in cardio-oncology, ensuring that patients receive optimal cancer treatment without compromising cardiovascular health.
The deadline for manuscript submission is 31 July 2026. All submissions will be peer-reviewed and published on a rolling basis upon acceptance, ensuring the rapid dissemination of high-impact research. Authors are strongly encouraged to submit their manuscripts as soon as they are ready.
Dr. Marco Tana
Guest Editor
Manuscript Submission Information
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Keywords
- cardiotoxicity
- CTRCD
- heart failure
- HFrEF
- HFpEF
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