TNF-Like Weak Inducer of Apoptosis Aggravates Left Ventricular Dysfunction after Myocardial Infarction in Mice
Figure 1
TWEAK directly promotes metabolic maladaptation by PGC-1α and OXPHOS gene inhibition in cardiomyocytes. (a) TWEAK dose dependently phosphorylated p65 without affecting cardiomyocyte apoptosis. TUNEL assay (b). Recombinant sTWEAK directly inhibited PGC-1α on mRNA and protein level in cardiomyocytes. Similar results could be observed by using an adenoviral vector containing TWEAK as an insert. (c) Likewise, OXPHOS genes like atp5O, ndufb5, cycs, and cox5b were also dose dependently inhibited by recombinant sTWEAK, which resulted in an overall increased ADP/ATP ratio ( for each experimental group).
