Research Paper Volume 13, Issue 10 pp 13788—13806

Redd1 knockdown prevents doxorubicin-induced cardiac senescence

Redd1 expression enhances Dox-induced cardiac senescence in vivo. (A, B) Representative images and corresponding quantitative expression analysis of Redd1 immunostaining in mouse heart tissues (n = 6 mice per group). (C, D) Immunofluorescence analysis of the effect of Redd1 overexpression and knockdown on p16INK4a and p21 expression in cardiac samples from Dox-treated mice. (E, F) Quantification of p16INK4a and p21 expression data (n = 6–8 per group). (G–J) Effect of Redd1 overexpression and knockdown on IL-1β, IL-6, IL-12, and TNFα mRNA in cardiac tissue from Dox-treated mice (n = 6–8 per group). Data are mean ± SEM. *p &p

Figure 6. Redd1 expression enhances Dox-induced cardiac senescence in vivo. (A, B) Representative images and corresponding quantitative expression analysis of Redd1 immunostaining in mouse heart tissues (n = 6 mice per group). (C, D) Immunofluorescence analysis of the effect of Redd1 overexpression and knockdown on p16INK4a and p21 expression in cardiac samples from Dox-treated mice. (E, F) Quantification of p16INK4a and p21 expression data (n = 6–8 per group). (GJ) Effect of Redd1 overexpression and knockdown on IL-1β, IL-6, IL-12, and TNFα mRNA in cardiac tissue from Dox-treated mice (n = 6–8 per group). Data are mean ± SEM. *p < 0.05 vs. the AAV9-NC group. &p < 0.05 vs. the AAV9-shNC group.