TNF-Like Weak Inducer of Apoptosis Aggravates Left Ventricular Dysfunction after Myocardial Infarction in Mice
Figure 6
Inhibition of intrinsic TWEAK activity improves survival after myocardial infarction in mice. (a) CD-1 mice were treated with neutralizing monoclonal antibodies against TWEAK or control IgG for 4 weeks after myocardial infarction. Anti-TWEAK treatment resulted in improved survival, preserved left ventricular function, and reduced expression of -MHC and BNP. These effects were independent of infarct size and the degree of left ventricular hypertrophy. (b) Anti-TWEAK treatment reduced the phosphorylation of p65 in the remote myocardium and preserved the expression of PGC-1α and OXPHOS genes like atp5O, ndufb5, cycs, and cox5b (molecular analysis for each group; functional analysis for each group).
