TNF-Like Weak Inducer of Apoptosis Aggravates Left Ventricular Dysfunction after Myocardial Infarction in Mice
Figure 4
sTWEAK promotes metabolic maladaptation in the remote myocardium after MI. (a) No significant changes in infarct size or interstitial fibrosis were noted in rsTWEAK-treated mice. Phosphorylation of Akt, GSK3, and ERK1/2 was significantly reduced in the myocardium of TWEAK-treated animals compared to vehicle-treated mice ( for NaCL and for rsTWEAK). (b) PGC-1α and PPARα expression in the remote myocardium after MI exhibited greater reductions when mice were treated with rsTWEAK. Likewise, expression of genes involved in oxidative metabolism (OXPHOS) like atp50, cycs, ndufb5, or cox5b was inhibited by treatment of animals with rsTWEAK ( for sham + NaCL, sham + TWEAK and LAD + NaCL, and LAD + rsTWEAK).
