针对致癌分子途径的激酶抑制剂 (KI) 彻底改变了癌症治疗。通过直接针对特定的肿瘤驱动激酶，靶向治疗与化疗相比副作用更少。尽管特异性增强，但许多靶向癌症疗法已经出现了心血管副作用，限制了癌症患者的长期结果。所有血管内壁的内皮细胞对于心血管健康至关重要，并且也暴露于循环水平的全身抗癌治疗。 KI 信号通路的正向和脱靶扰动都会导致内皮功能障碍，从而导致心血管毒性。因此，内皮是心血管毒性的潜在来源，也是预防的治疗靶点。在这篇综述中，我们检查了 KI 诱导的内皮细胞功能障碍作为血管内皮生长因子抑制剂、BCR-Abl KI、Bruton 酪氨酸抑制剂的心血管毒性机制的证据，以及有关新型 KI 的内皮毒性的新信息。

Kinase inhibitors (KIs) targeting oncogenic molecular pathways have revolutionized cancer therapy. By directly targeting specific tumor-driving kinases, targeted therapies have fewer side effects compared with chemotherapy. Despite the enhanced specificity, cardiovascular side effects have emerged with many targeted cancer therapies that limit long-term outcomes in patients with cancer. Endothelial cells lining all blood vessels are critical to cardiovascular health and are also exposed to circulating levels of systemic anticancer therapies. Both on- and off-target perturbation of signaling pathways from KIs can cause endothelial dysfunction, resulting in cardiovascular toxicity. As such, the endothelium is a potential source, and also a therapeutic target for prevention, of cardiovascular toxicity. In this review, we examine the evidence for KI-induced endothelial cell dysfunction as a mechanism for the cardiovascular toxicities of vascular endothelial growth factor inhibitors, BCR-Abl KIs, Bruton tyrosine inhibitors, and emerging information regarding endothelial toxicity of newer classes of KIs.