Sorafenib-induced cardiovascular toxicity: A cause for concern

Abstract

Sorafenib, a multi-target tyrosine kinase inhibitor, is primarily used to manage hepatocellular carcinoma, advanced renal cell carcinoma, and differentiated thyroid cancer. Although this drug extends patient survival and slows tumor progression, its cardiovascular toxicity substantially impacts of quality of life. Effective the prevention and treatment of the resulting complications are needed. The mechanisms underlying of sorafenib-induced cardiovascular toxicity are complex, and remain incompletely understood despite extensive research. In this review, we discuss the incidence of sorafenib-induced cardiovascular toxicity, including hypertension, thromboembolism, and heart failure in clinical settings. We also summarize current research on the underlying mechanisms, such as ferroptosis, necroptosis, autophagy, mitochondrial damage, and endoplasmic reticulum stress. Additionally, we explore studies regarding the protective effects of various drugs against sorafenib-induced cardiovascular toxicity. This in-depth synthesis of data regarding the clinical manifestations and mechanisms of sorafenib-induced cardiotoxicity provides a valuable scientific foundation for developing therapeutic drugs to combat these adverse effects.