IL‐17 in intervertebral disc degeneration: Mechanistic insights and therapeutic implications

Abstract Intervertebral disc degeneration (IDD) serves as an independent risk factor for lower back pain and is closely associated with spinal musculoskeletal disorders, including lumbar disc herniation, radiculopathy, and myelopathy. Interleukin‐17 (IL‐17), also named IL‐17A, is a critical signature cytokine of T‐helper 17 cells. Upon binding to the IL‐17 receptor A/C heterodimeric complex, IL‐17 can trigger multiple signal transduction pathways to stimulate gene transcription and increase messenger RNA stability. IL‐17 expression is significantly increased in degenerative disc tissue and shows a positive correlation with disease severity. IL‐17 has been shown to accelerate the development of IDD by promoting extracellular matrix degradation, enhancing inflammatory response, inducing neoangiogenesis, and inhibiting nucleus pulposus cell autophagy and proliferation. Targeting IL‐17 represents a novel and promising approach for the therapeutic intervention of IDD. In this review, we summarized the recent progression about the role of IL‐17 in IDD and highlighted its therapeutic implications.