Therefore, it can be predicted that when AOPPs start to appear in the degenerated disc tissue, it will activate the high expression of NOX4, induce AF cell senescence through the MAPK pathway, and continuously secrete IL-1β and TNF-α, which together with the activation of NOX4 aggravate oxidative stress on the one hand (Li et al., 2021), and recruit immune cells on the other, both of which work together to convert the accumulated albumin in the disc into AOPPs. Here, IL1B is linked to atrial fibrillation.