Fig. 5.

Inhibition of activin type II receptor (ACTRII)/TGFβ receptor (TGFBR) may improve calcium cycling and prevents unfolded protein response (UPR) after experimental myocardial infarction (MI). A: cardiac protein levels of increased sarco/endoplasmic reticulum Ca²⁺-ATPase (SERCA2a) and representative blots of sham and MI mice treated with vehicle, Myo-Fc, or a combination of follistatin and a TGFβ receptor inhibitor (Fol + TGFi); n ≥ 8 mice/group. B: cardiac gene expression levels of binding immunoglobulin protein (BiP); n = 5 mice/group. C and D: spliced/total ratio of X-box binding protein (XBP1; C) and total and phosphorylated eukaryotic translation initiation factor-2α (eIf2α) and representative blots (D), n ≥ 8 mice/group. E and F: cardiac gene expression levels of activating transcription factor 4 (ATF4; E) and C/EBP homologous protein (CHOP; F); n = 5 mice/group. G: total and phosphorylated eIF2α and representative blots of AC16 cultured cardiomyocytes transfected with nontargeting or MSTN siRNA. Results are expressed as %nontarget; n = 4/condition. *P < 0.05 by 2-way ANOVA (A–F) or t-test (G).