Intervertebral disc degeneration (IDD) is a major cause of low back pain (LBP), and the pathogenesis remains unknown. Recently, an autoregulating circadian rhythm was identified in intervertebral discs (IVDs), the abolition of which led to IDD. The genetic disruption of the mouse IVD molecular clock, specifically through the disruption of Bmal1, predisposes mice to IDD. However, the precise role of circadian gene Bmal1 in IDD remain elusive. Using a tandem mass tag (TMT)-based quantitative proteomics approach, we characterized the proteomes and phosphoproteomes of rat nucleus pulposus cells (NPCs) treated with Bmal1 shRNA or its negative control lentivirus.