Additionally, our results suggest that premature senescence in the DM1 model cells is associated with mitochondrial dysfunction and ROS production, leading to the upregulation of secreted mediators IGFBP3 and PAI-1 and cell cycle regulators p16, p21, and possibly p53 (Figure 6). The gene discussed is CDKN1A; the disease is myotonic dystrophy type 1.