Objective    To explore the contribution of the c-Jun N-terminal protein kinase (JNK) signaling pathway to cardiac myocyte apoptosis in mouse congestive heart failure due to myocardial infraction.     Methods    The mouse heart failure model was induced by acute myocardial infarction through ligating the left coronary artery. Thirty-two health male mice were randomly divided into 4 groups: sham operated group

2-week postoperative group

4-week postoperative group and 6-week postoperative group. The ventricular dilatation and left ventricular function were assessed by echocardiography. The expressions of GRP78

JNK and phosphorylated JNK were assessed by Western blot assay. The cardiac myocyte apoptosis were assessed by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL).     Results    Compared with the sham group

cardiac expression of endoplasmic reticulum chaperones GRP78 and phosphorylated JNK were significantly up-regulated in the operation groups (P0.05). The number of TUNEL positive cells were markedly increased in the operation group compared with the sham group (P0.05).     Conclusion    These findings suggest that the CNK signaling pathway partly mediates cardiac myocyte apoptosis in mouse congestive heart failure due to myocardial infraction via endoplasmic reticulum stress.