Examination of its pathophysiology points to a strong connection of intervertebral disc degeneration with ferroptosis, a regulated cell death that occurs through an iron-dependent mechanism and the accumulation of reactive oxygen species. Hemoglobin, an oligometalloprotein, consists of four iron-carrying heme molecules and a globin molecule consisting of two alpha-two beta polypeptide chains. Increased heme values, especially as a result of neovascularization in the herniated nucleus pulposus, can accelerate degeneration by inducing cytotoxicity and ferroptosis. This study aimed to focus on the role of ferroptosis in intervertebral disc degeneration.