Abstract: Intervertebral disc degeneration is an important pathological basis of chronic low back pain. Its development involves multiple processes, including cellular stress, persistent inflammation, extracellular matrix degradation, aberrant neurovascular ingrowth, and impaired tissue repair. In recent years, increasing attention has been paid to the role of cellular senescence and the senescence-associated secretory phenotype(SASP) in intervertebral disc degeneration and related pain. Oxidative stress, abnormal mechanical loading, inflammatory stimulation, metabolic disturbance, and an acidic microenvironment may activate classical senescence regulatory axes, including the p53/p21/Rb and p16INK4a/Rb pathways, thereby driving intervertebral disc cells into a state of stable proliferative arrest and functional decline. Senescent cells further release pro-inflammatory factors, chemokines, and matrix-degrading molecules through SASP, contributing to inflammatory amplification, extracellular matrix disruption, impaired repair, and pain-related microenvironmental changes. Mitochondrial dysfunction, impaired autophagy and mitophagy, and metabolic remodeling are closely coupled with cellular senescence and jointly participate in the formation and maintenance of the degenerative microenvironment. Current research has gradually shifted from identifying senescent cells in degenerative discs to clarifying pathogenic senescent cell subpopulations, key SASP components, and targetable regulatory nodes. This review summarizes the inducing factors of intervertebral disc cell senescence, the pathological mechanisms by which SASP mediates disc degeneration and pain-related microenvironmental changes, the senescence characteristics of different disc tissue components, and emerging targeted interventions, aiming to provide a reference for mechanistic studies and disease-modifying therapeutic strategies for intervertebral disc degeneration and related pain.