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<p>Cancer treatment-related cardiotoxicity (CTRC) encompasses a spectrum of cardiovascular complications associated with chemotherapy, targeted therapy, and radiotherapy. This review synthesizes recent mechanistic insights to delineate distinct pathological pathways: anthracyclines provoke oxidative mitochondrial damage and disrupt cardiomyocyte iron homeostasis; HER2-targeted therapies inhibit the PI3K-Akt survival pathway, compromising contractile function and calcium regulation; tyrosine kinase inhibitors impair VEGF and PDGF signaling, inducing endothelial dysfunction and microvascular rarefaction; immune checkpoint inhibitors activate T-cell-mediated myocarditis; and thoracic radiation initiates endothelial inflammation followed by TGF-β–dependent fibrotic remodeling. These mechanism-specific injuries follow a characteristic clinical sequence, with arrhythmias and myocarditis emerging acutely, subclinical contractile dysfunction developing within months, and overt heart failure or vascular stenosis manifesting years post-treatment. We highlight the critical roles of advanced imaging and biomarker-based surveillance in early detection, and underscore evidence-based cardioprotective interventions that maintain anticancer efficacy while mitigating cardiovascular risk.</p>

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Cancer treatment-related cardiotoxicity, molecular mechanism, challenges, and research trends

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年2月4日

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  • Jia-yuan Ling,
  • Lun-ming Wen,
  • Kangmin Liu,
  • Wei-qing Yuan,
  • Yi-ming Zhong,
  • Ping Lai,
  • Yong-ling Liao

摘要

Cancer treatment-related cardiotoxicity (CTRC) encompasses a spectrum of cardiovascular complications associated with chemotherapy, targeted therapy, and radiotherapy. This review synthesizes recent mechanistic insights to delineate distinct pathological pathways: anthracyclines provoke oxidative mitochondrial damage and disrupt cardiomyocyte iron homeostasis; HER2-targeted therapies inhibit the PI3K-Akt survival pathway, compromising contractile function and calcium regulation; tyrosine kinase inhibitors impair VEGF and PDGF signaling, inducing endothelial dysfunction and microvascular rarefaction; immune checkpoint inhibitors activate T-cell-mediated myocarditis; and thoracic radiation initiates endothelial inflammation followed by TGF-β–dependent fibrotic remodeling. These mechanism-specific injuries follow a characteristic clinical sequence, with arrhythmias and myocarditis emerging acutely, subclinical contractile dysfunction developing within months, and overt heart failure or vascular stenosis manifesting years post-treatment. We highlight the critical roles of advanced imaging and biomarker-based surveillance in early detection, and underscore evidence-based cardioprotective interventions that maintain anticancer efficacy while mitigating cardiovascular risk.