This review explores the mechanisms and treatment implications of sorafenib-induced cardiovascular toxicity. Sorafenib, a tyrosine kinase inhibitor (TKI) targeting the vascular endothelial growth factor receptor (VEGFR), is widely used for treating various cancers, including hepatocellular carcinoma (HCC) and renal cell carcinoma (RCC). While effective in prolonging life, sorafenib can cause adverse cardiovascular effects such as hypertension, thromboembolism, cardiac ischemia, and left ventricular dysfunction. The review discusses the underlying mechanisms, including endothelial dysfunction, mitochondrial dysfunction, endoplasmic reticulum stress, dysregulated autophagy, and ferroptosis. It also highlights potential treatment strategies, such as antioxidants and renin-angiotensin system inhibitors, and the association between sorafenib-induced hypertension and treatment efficacy in cancer patients. Emerging research suggests a link between sorafenib-induced glycolysis and drug resistance, emphasizing the need for further investigation. Understanding these mechanisms is crucial for optimizing sorafenib therapy and minimizing cardiovascular risks in cancer patients.This review explores the mechanisms and treatment implications of sorafenib-induced cardiovascular toxicity. Sorafenib, a tyrosine kinase inhibitor (TKI) targeting the vascular endothelial growth factor receptor (VEGFR), is widely used for treating various cancers, including hepatocellular carcinoma (HCC) and renal cell carcinoma (RCC). While effective in prolonging life, sorafenib can cause adverse cardiovascular effects such as hypertension, thromboembolism, cardiac ischemia, and left ventricular dysfunction. The review discusses the underlying mechanisms, including endothelial dysfunction, mitochondrial dysfunction, endoplasmic reticulum stress, dysregulated autophagy, and ferroptosis. It also highlights potential treatment strategies, such as antioxidants and renin-angiotensin system inhibitors, and the association between sorafenib-induced hypertension and treatment efficacy in cancer patients. Emerging research suggests a link between sorafenib-induced glycolysis and drug resistance, emphasizing the need for further investigation. Understanding these mechanisms is crucial for optimizing sorafenib therapy and minimizing cardiovascular risks in cancer patients.