椎间盘由髓核、纤维环和软骨终板组成,对维持脊柱正常生理功能至关重要。椎间盘退变(intervertebral disc degeneration,IDD)是导致腰背痛等脊柱退行性疾病的主要病理基础,给人们的健康状况造成极大的困扰。然而目前对IDD的分子机制仍然缺乏清晰的了解，导致缺乏有效的靶向干预措施。RAS同源家族成员A(RAS homolog family member A, RhoA)/Rho相关蛋白激酶(Rho-associated protein kinase, ROCK)信号通路是调节细胞收缩、迁移和生长的经典通路。其被激活后可参与调控细胞骨架重塑、细胞外基质代谢、生物钟节律、细胞表型改变、细胞衰老及死亡等环节,进而影响IDD的病理进程。深入探究RhoA/ROCK信号通路在IDD中的作用,不仅能揭示疾病发生的分子生物学机制,也有望为研发靶向该通路的治疗策略提供理论依据。

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.