Li Xin, Lin Yongping, Lin Song, Huang Jiayi, Ruan Zhongbao
Department of Cardiology, The Affiliated Taizhou People's Hospital of Nanjing Medical University, Taizhou School of Clinical Medicine, Nanjing Medical University, Taizhou, China.
Front Pharmacol. 2024 Aug 15;15:1404692. doi: 10.3389/fphar.2024.1404692. eCollection 2024.
Epidermal Growth Factor Receptor-Tyrosine Kinase Inhibitors (EGFR-TKIs) are a class of oral targeted anticancer drugs that have been demonstrated to significantly inhibit tumor progression and improve clinical prognosis in patients diagnosed with EGFR-mutated tumors, particularly in those with non-small cell lung cancer. However, the sustained usage of EGFR-TKIs may cause potential cardiotoxicity, thus limiting their applicability. The primary objective of this review is to systematically analyze the evolving landscape of research pertaining to EGFR-TKI-induced cardiotoxicity and elucidate its underlying mechanisms, such as PI3K signaling pathway inhibition, ion channel blockade, oxidative stress, inflammatory responses, and apoptosis. Additionally, the review includes an exploration of risk assessment for cardiotoxicity induced by EGFR-TKIs, along with management and response strategies. Prospective research directions are outlined, emphasizing the need for more accurate predictors of cardiotoxicity and the development of innovative intervention strategies. In summation, this review consolidates recent research advances, illuminates the risks associated with EGFR-TKI-induced cardiac toxicity and presents crucial insights for refining clinical dosage protocols, optimizing patient management strategies, and unraveling the intricate mechanisms governing EGFR-TKI-induced cardiotoxicity.
表皮生长因子受体酪氨酸激酶抑制剂(EGFR-TKIs)是一类口服靶向抗癌药物,已被证明能显著抑制肿瘤进展,并改善诊断为EGFR突变肿瘤患者的临床预后,尤其是非小细胞肺癌患者。然而,持续使用EGFR-TKIs可能会导致潜在的心脏毒性,从而限制了它们的适用性。本综述的主要目的是系统分析与EGFR-TKI诱导的心脏毒性相关的研究进展,并阐明其潜在机制,如PI3K信号通路抑制、离子通道阻滞、氧化应激、炎症反应和细胞凋亡。此外,该综述还探讨了EGFR-TKIs诱导的心脏毒性的风险评估,以及管理和应对策略。概述了前瞻性研究方向,强调需要更准确的心脏毒性预测指标和创新干预策略的开发。总之,本综述整合了近期的研究进展,阐明了EGFR-TKI诱导的心脏毒性相关风险,并为完善临床用药方案、优化患者管理策略以及揭示EGFR-TKI诱导心脏毒性的复杂机制提供了关键见解。