Molecular mechanisms of hypertension and heart failure due to antiangiogenic cancer therapies.

摘要

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.