Abstract: Antitumor drug-related hypertension is a common and important complication in cancer therapy, yet its underlying mechanisms have not been fully elucidated. Studies indicate that anti-angiogenic drugs, small molecule tyrosine kinase inhibitors, and other anti-tumor drugs can increase the risk of hypertension through mechanisms such as vascular endothelial growth factor inhibition, reninangiotensin system activation, renal injury and sodium retention. This review summarizes the pathogenesis and management strategies of antitumor drug-related hypertension, aiming to provide insights for clinical practice and future research.