Fig. 5: Exercise-induced senescence is observed in normal mice.
a Protocols for the CIM model and exercise intervention. b The number of FAPs in sedentary (n = 3) vs. exercise control mice (n = 5), and sedentary (n = 5) vs. exercise CIM mice (n = 5). c Relative mRNA expression of senescence-related genes (Cdkn2a, Trp53, and P21), pro-regenerative genes (Tnfaip6 and Il33), and pro-fibrotic genes (Tgfb1 and Acta1) in FAPs from sedentary control (n = 3), exercise control (n = 5), sedentary CIM (n = 3), and exercise CIM (n = 5) mice. d, g Flow cytometric analysis of p16INK4A, p53, phospho-p38 MAPK, and phospho-p65 NF-κB in FAPs from sedentary control, exercise control, sedentary CIM, and exercise CIM mice (n = 3 in each group). d Representative p16INK4A and p53 histograms from n = 3 replicates, and e quantification of the percentage of p16INK4A+or p53+ FAPs. f Representative phospho-p38 MAPK and phospho-p65 NF-κB contour plot from n = 3 replicates, and g quantification of the percentages of phospho-p38 MAPK+ and phospho-p65 NF-κB+ FAPs. Quantitative data are shown as means as well as medians with IQRs and 1.5 times the IQR, and are displayed by dot plots and box and whisker plots. P values were determined by the two-tailed Student’s t test (*P < 0.05, **P < 0.001).
