TNF-like weak inducer of apoptosis aggravates left ventricular dysfunction after myocardial infarction in mice.

ABSTRACT:

Background

TNF-like weak inducer of apoptosis (TWEAK) has recently been shown to be potentially involved in adverse cardiac remodeling. However, neither the exact role of TWEAK itself nor of its receptor Fn14 in this setting is known.

Aim of the study

To analyze the effects of sTWEAK on myocardial function and gene expression in response to experimental myocardial infarction in mice.

Results

TWEAK directly suppressed the expression of PGC-1α and genes of oxidative phosphorylation (OXPHOS) in cardiomyocytes. Systemic sTWEAK application after MI resulted in reduced left ventricular function and increased mortality without changes in interstitial fibrosis or infarct size. Molecular analysis revealed decreased phosphorylation of PI3K/Akt and ERK1/2 pathways associated wit

SUBMITTER: Jarr KU 

PROVIDER: S-EPMC3945977 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature