As the core pathological basis of chronic low back pain and spinal dysfunction, intervertebral disc degeneration (IVDD) is not caused solely by mechanical wear and tear, but rather is the result of a progressive process in which mechanical imbalances and biological dysregulation are deeply intertwined. The introduction of the concept of "inflammaging" provides a new dimension for elucidating its complex evolutionary law. Studies have shown that the pathological evolution of IVDD is not a stacking of isolated events, but a multi-dimensional molecular cascade response driven by inflammatory aging. Internal and external stress triggers the continuous release of the senescence-associated secretory phenotype (SASP) by inducing cells to enter the aging process, which not only reshapes the local immune microenvironment, but also leads to the gradual loss of the original immune privilege of the intervertebral disc. Under the action of chronic low-grade inflammation, cell metabolic reprogramming is becoming more and more significant: excessive lactic acid accumulation forms a feed-forward cycle of "microenvironment acidification-inflammation cascade-matrix degradation" by activating acid-sensitive ion channels. With the progression of the disease, the abnormal activation of the transforming growth factor-β signaling pathway further promotes the phenotypic transformation of cells, resulting in the transformation of the elastic matrix to pathological fibrosis, which eventually leads to the loss of spinal motor unit function. In view of the above pathological processes, this paper systematically reviews the cutting-edge intervention strategies to block the cascade reaction, including the use of senolytic drugs to target the removal of senescent cells to block the source of inflammation, the targeting of the inhibition of SASP paracrine effects with the help of functional carriers, and the reshaping of matrix homeostasis with the help of responsive hydrogels. In-depth analysis of the molecular cascade mechanism triggered by inflammatory aging and synergistic biomaterial technology to block the pathological circulation can provide important theoretical support for early intervention and tissue regeneration and repair of IVDD.