Department of Cardiology, University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Unit 1101, Houston, TX 77030, USA.
Heart Fail Clin. 2011 Jul;7(3):299-311. doi: 10.1016/j.hfc.2011.03.004.
Targeted antiangiogenic cancer therapies have revolutionized the treatment of highly vascularized cancers such as metastatic renal cell carcinoma and gastrointestinal stromal tumors. Such agents act by inhibiting the actions of proangiogenic growth factors and their receptor tyrosine kinases, which are known to be overexpressed in cancer. However, these factors also play an important role in normal cardiovascular physiology. This article summarizes the incidences of cardiovascular toxicities (namely hypertension and heart failure) associated with the most commonly used antiangiogenic therapies, and then presents data from preclinical and clinical studies to provide some insight into the underlying molecular mechanisms.
靶向抗血管生成的癌症治疗方法已经彻底改变了转移性肾细胞癌和胃肠道间质瘤等高度血管化癌症的治疗方式。这些药物通过抑制促血管生成生长因子及其受体酪氨酸激酶的作用来发挥作用，这些因子在癌症中已知过度表达。然而，这些因子在正常心血管生理学中也起着重要作用。本文总结了与最常用的抗血管生成治疗相关的心血管毒性（即高血压和心力衰竭）的发生率，然后介绍了临床前和临床研究的数据，为潜在的分子机制提供了一些见解。
