Intervertebral disc degeneration (IVDD) is responsible for about 40% of cases of low back pain, the leading cause of disability worldwide. Researchers in China report on a mechanism of IVDD progression whereby aberrant genomic DNA damage promotes senescence of nucleus pulposus (NP) cells, revealing a potential target that could improve IVDD outcomes.

Intervertebral discs (IVDs) are avascular fibrocartilaginous tissues located between adjacent spinal vertebrae and are composed of three distinct components: a central gelatinous NP, a collagen-rich annulus fibrosus, and hyaline cartilage endplates. Native NP cells are involved in regulating extracellular matrix homeostasis and maintaining the gelatinous properties of NP tissue. “The accumulation of senescent [NP] cells caused by aging and other factors is a distinctive hallmark of the initiation and progression of IVDD, which leads to impaired self-repair capacity, degenerative biomechanical modifications, discogenic pain and disability,” explains Cao Yang, an author on the new study. “Understanding the molecular mechanisms that occur in senescent NP cells under cellular stress might provide new targets to improve treatment of IVDD.”