Abstract
Ferroptosis is an iron-dependent programmed cell death characterized by lipid peroxidation. Ferroptosis plays a key role in the dysfunction of vascular endothelial cells (VECs), which may promote pathological vascular damage through oxidative stress, inflammatory response, and barrier integrity destruction. The pathogenesis of vertebral artery (VA) type cervical spondylosis (CSA) is complex. Cervical degeneration and other factors can induce ferroptosis of VA VECs. This review systematically reviews the cutting-edge research results on the biological characteristics of ferroptosis, analyzes its molecular mechanism in the regulation of VECs function, and systematically discusses its internal relationship with CSA pathogenesis. This study provides a new perspective on the pathogenesis of CSA, as well as a new theoretical basis and potential intervention targets for developing targeted treatment strategies and disease prevention.