The intervertebral disc consists of the nucleus pulposus, annulus fibrosus, and cartilage endplates, and plays a crucial role in maintaining the normal physiological function of the spine. Intervertebral disc degeneration (IDD) is the primary pathological basis for spinal degenerative diseases such as low back pain, imposing a significant health burden on individuals. However, the molecular mechanisms underlying IDD remain poorly understood, leading to a lack of effective targeted intervention strategies. The RAS homolog family member A (RhoA)/Rho-associated protein kinase (ROCK) signaling pathway is a classical pathway regulating cell contraction, migration, and growth. Upon activation, it participates in regulating cytoskeletal remodeling, extracellular matrix metabolism, circadian rhythms, cellular phenotype changes, cellular senescence, and cell death, thereby influencing the pathological progression of IDD. Elucidating the role of the RhoA/ROCK signaling pathway in IDD not only provides insight into the molecular mechanisms of disease development, but also offers a theoretical basis for developing therapeutic strategies targeting this pathway.