SIRT1-autophagy axis may inhibit oxidative stress-induced ferroptosis in human nucleus pulposus cells

Low back pain (LBP) is a common problem that causes enormous socioeconomic burden worldwide. Intervertebral disc degeneration (IDD) is considered to be a major cause of LBP. The specific mechanism of IDD is not fully understood; however, the decrease in the number of nucleus pulposus (NP) cells and loss of function are thought to be the main reasons for IDD. Therefore, the study of NP cell apoptosis plays an important role in the study of IDD. Autophagy, as a major intracellular lysosome-dependent degradation process, plays a key role in maintaining intracellular homeostasis and resisting environmental pressure, which may be a potential therapeutic target for IDD. Ferroptosis is a type of iron-dependent regulated cell death caused by disruption that occurs when oxidative stress and antioxidant defenses interact, and is subsequently driven by lipid peroxidation and plasma membrane ruptures. However, the potential links between autophagy and ferroptosis in IDD are unknown. Herein we postulate that SIRT1-autophagy axis can inhibit oxidative stress-induced NP cell ferroptosis. These findings may aid the development of novel therapeutic approaches for IDD treatment.