| First Author | Yang H | Year | 2015 |
| Journal | Apoptosis | Volume | 20 |
| Issue | 4 | Pages | 512-22 |
| PubMed ID | 25608996 | Mgi Jnum | J:315357 |
| Mgi Id | MGI:6830205 | Doi | 10.1007/s10495-015-1089-1 |
| Citation | Yang H, et al. (2015) Activation of NOD1 by DAP contributes to myocardial ischemia/reperfusion injury via multiple signaling pathways. Apoptosis 20(4):512-22 |
| abstractText | NOD1 is a member of nucleotide-binding oligomerization domain-like receptors family that participates in many inflammatory processes. Previous studies demonstrated that NOD1 plays an important role in inflammatory cardiovascular diseases. However, its role in myocardial ischemia/reperfusion (I/R) injury remains unknown. The present study investigate whether NOD1 is involved in the pathogenesis of mouse myocardial I/R injury and the underlying mechanisms. Administration of NOD1 ligand (DAP) significantly enhanced myocardial I/R injury, as demonstrated by increased infarct size, the number of TUNEL-positive nuclei, caspase-3 activity, the infiltration of Mac-2- and IL-6-positive cells as compared with untreated heart or cardiomyocytes after I/R injury. In contrast, knockdown of NOD1 by siRNA markedly attenuated mimetic I/R induced cardiomyocyte apoptosis in vitro, indicating that NOD1 enhanced myocardial I/R injury partially through direct heart effects. These effects were partially associated with activation of JNK, p38 MAPK and NF-kappaB signaling pathways. Taken together, these results provide the first evidence that activation of intracellular sensor NOD1 enhances myocardial I/R injury and may provide novel therapeutic target for ameliorating the ischemic heart diseases. |
