The role of IL-1β and TNF-α in intervertebral disc degeneration

Low back pain (LBP), a prevalent and costly disease around the world, is predominantly caused by intervertebral disc (IVD) degeneration (IDD). LBP also presents a substantial burden to public health and the economy. IDD is mainly caused by aging, trauma, genetic susceptibility, and other factors. It is closely associated with changes in tissue structure and function, including progressive destruction of the extracellular matrix (ECM), enhanced senescence, disc cell death, and impairment of tissue biomechanical function. The inflammatory process, exacerbated by cytokines interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha), are considered to be the key mediators of IDD and LBP. IL-1 beta and TNF-alpha are the most important proinflammatory cytokines, as they have powerful proinflammatory activities and can promote the secretion of a variety of proinflammatory mediators. They are also upregulated in the degenerative IVDs, and they are closely related to various pathological IDD processes, including inflammatory response, matrix destruction, cellular senescence, autophagy, apoptosis, pyroptosis, and proliferation. Therefore, anti-IL-1 beta and anti-TNF-alpha therapies may have the potential to alleviate disc degeneration and LBP. In this paper, we reviewed the expression pattern and signal transduction pathways of IL-1 beta and TNF-alpha, and we primarily focused on their similar and different roles in IDD. Because IL-1 beta and TNF-alpha inhibition have the potential to alleviate IDD, an in-depth understanding of the role of IL-1 beta and TNF-alpha in IDD will benefit the development of new treatment methods for disc degeneration with IL-1 beta and TNF-alpha at the core.