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. 2021 Sep 8;6(17):e148375. doi: 10.1172/jci.insight.148375

Figure 1. Failing human hearts and aged mouse hearts show reduced MG53 and increased p65 activation.

Figure 1

(A) Western blot of MG53, total p65 (t-p65), and phosphorylated p65 (p-p65) in nonfailing human hearts (NFHs, n = 13) and failing human hearts (FHs, n = 15). GAPDH serves as loading control. (B) Quantification of MG53, t-p65, and p-p65 in NFH and HF tissues. (C) Inverse correlation between MG53 and p-p65 expression in human heart tissues. (D) Left ventricular ejection fraction (LV EF) in young (3 months, n = 15) and aged (24 months, n = 14) mice. (E) Western blot for MG53, p-p65, p65 in young mouse hearts (YH, 3 months, n = 4) and aged (AH, 24 months, n = 4) mouse hearts. (F) Quantification of MG53, t-p65, and p-p65 expression in young and aged mouse hearts. Data are expressed as mean ± SEM. Differences were analyzed for significance by unpaired t test; P values are presented in the individual panels.