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April 3, 2026Balkan Medical Journal0 citationsOpen Access

Cardio-Oncology in 2025: From Molecular Mechanisms to Clinical Practice

KKK Keramida

Key Points

  • The aim is to outline key developments in cardio-oncology, focusing on cardiotoxicity mechanisms and potential protective strategies.
  • Examined mechanistic discoveries and clinical practice advancements in cardio-oncology.
  • Utilized in vivo and in vitro models to study doxorubicin-induced cardiotoxicity.
  • Identified STAT3's role in ferroptosis related to anthracycline therapies.
  • Investigated the effects of liraglutide on myocardial dysfunction.
  • Reframed anthracycline cardiotoxicity as a ferroptosis-driven process.
  • Demonstrated that liraglutide reduces doxorubicin-induced myocardial dysfunction.
  • Highlighted the potential of GLP-1 receptor agonists as cardioprotective agents in cancer treatment.

Abstract

The year 2025 marked an important step forward for cardio-oncology, with advances spanning mechanistic discovery, prevention-oriented trials, risk stratification, and expert consensus statements that collectively signal a transition toward precision cardiovascular (CV) care.This editorial presents a focused narrative selection of highimpact 2025 contributions-covering anthracycline (AC)/human epidermal growth factor receptor 2 (HER2) therapies related cardiotoxicity, immune checkpoint inhibitors (ICIs), prevention strategies, survivorship, and key statements-rather than a systematic review (Figure 1); several practice-relevant areas (e.g., radiationassociated CV disease, thrombosis, and arrhythmias) remain outside the scope of the present discussion.At the preclinical level, one of the most informative advances was the reframing of AC cardiotoxicity as a ferroptosis-driven process.Gao et al. 1 employed complementary in vivo and in vitro models of doxorubicin-induced cardiotoxicity, including a chronic murine model and cultured cardiomyocytes, to investigate both functional and molecular endpoints.The investigators identified STAT3 as a central regulator of ferroptotic susceptibility.Importantly, pharmacological intervention with liraglutide consistently attenuated doxorubicininduced myocardial dysfunction and ferroptotic signaling, thereby repurposing GLP-1 receptor agonists-already widely used in cardiometabolic disease-as potential cardioprotective agents in oncology.

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K Keramida (2026) studied this question.

synapsesocial.com/papers/69cf5e745a333a821460cdffhttps://doi.org/10.4274/balkanmedj.galenos.2026.2026-1-183
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