Skip to main content
. 2019 Jul 8;10(7):520. doi: 10.1038/s41419-019-1749-0

Fig. 7. Protein p38-induced activation of the ER stress pathway is involved in pathological cardiac hypertrophy.

Fig. 7

a Representative western blot of the activity of GRP78, eIF2α, IRE1α, CHOP, and ATF6 in mice hearts from indicated groups. b Statistical diagrams of GRP78, eIF2α, IRE1α, CHOP, and ATF6 protein expression in mice hearts from indicated groups (n = 6 mice per group). c Representative western blot of the activity of GRP78, eIF2α, IRE1α, CHOP, and ATF6 in mice hearts from indicated groups. d Statistical diagrams of GRP78, eIF2α, IRE1α, CHOP, and ATF6 protein expression in mice hearts from indicated groups (n = 6 mice per group). e, f Representative immunofluorescence images of murine heart sections stained with GRP78 (red) and DAPI (blue) in the hearts of mice with different genotypes (WT, Ctrp3-KO, and LV-CTRP3) 4 weeks after sham treatment or TAC surgery (n = 5–6 mice per group). g Representative western blot (left), and quantification (right) of GRP78, eIF2α, IRE1α, CHOP, and ATF6 in the hearts of mice from the indicated groups (n = 5 mice per group). The data were analyzed by one-way ANOVA. b, d *p < 0.05, **p < 0.01 vs. SHAM, #p < 0.05 vs. TAC. g *p < 0.05 and #p < 0.05 between indicated groups. In the bar graphs, the data are presented as the mean ± SEM