Advances in cancer therapy, including anthracyclines (e.g., doxorubicin [DOX]) and immune checkpoint inhibitors (ICIs), have significantly improved survival rates. However, their capacity to inflict direct myocardial damage remains a critical clinical concern. DOX-induced cardiotoxicity is closely linked to oxidative stress, mitochondrial dysfunction, and ferroptosis, mediated via topoisomerase IIβ inhibition and impaired autophagy. ICIs, while transformative in oncology, can trigger immune-related myocarditis through T-cell activation against cardiac antigens such as troponin and myosin. Despite these recognised risks, the molecular mechanisms driving cardiomyocyte injury — ROS generation, DNA damage, regulated cell death pathways, and immune checkpoint dysregulation (PD-1/PD-L1, CTLA-4) — remain not fully understood.

Clinical translation is further limited by a lack of cardiomyocyte-specific predictive biomarkers, incomplete characterisation of genetic susceptibility (e.g., RARG and ABCB1 polymorphisms), and limited understanding of how inflammatory cytokines (IL-6, TNF-α) drive maladaptive cardiac remodelling at the cellular level. Closing these gaps is essential to design interventions that protect the myocardium without compromising oncologic efficacy.

This Research Topic aims to consolidate mechanistic, translational, and early clinical evidence on cancer therapy–induced myocardial injury, with a focus on actionable molecular targets. We welcome contributions across the following areas:

• Regulated cell death pathways in cardiomyocytes — ferroptosis, pyroptosis, apoptosis, and autophagy in the context of DOX, ICIs, and other myocardial-toxic agents
• Cardiomyocyte-specific biomarkers — circulating microRNAs, high-sensitivity troponin, and emerging molecular signatures for early detection of myocardial injury
• Targeted cardioprotective interventions — NLRP3 inflammasome inhibitors, dexrazoxane and next-generation analogs, and mechanism-based pharmacological strategies
• Genetic and molecular susceptibility — pharmacogenomic predictors of cardiomyocyte vulnerability and individualised risk
•Translational and survivorship insights — bridging preclinical cardiomyocyte models to long-term myocardial outcomes in cancer survivors

By fostering multidisciplinary collaboration between oncologists, cardiologists, molecular biologists, and translational researchers, this collection aims to advance mechanism-based, cardiomyocyte-targeted strategies that balance oncologic efficacy with myocardial safety, supporting the integration of cardio-oncology into precision medicine frameworks.

We welcome original research, mechanistic reviews, and perspective articles. Submissions should bridge preclinical findings to clinical applications, with emphasis on methodological rigour and direct relevance to cardiomyocyte biology.

Are you interested in contributing a manuscript to this Research Topic?

Mechanisms and Management of Cancer Therapy-Induced Myocardial Injury