Pub. Date : 2019 Jan
PMID : 30338935
4 Functional Relationships(s)Download |
Sentence | Compound Name | Protein Name | Organism |
| 1 | Cardiac-specific Mst1 deficiency inhibits ROS-mediated JNK signalling to alleviate Ang II-induced cardiomyocyte apoptosis. | Reactive Oxygen Species | mitogen-activated protein kinase 8 | Homo sapiens |
| 2 | In vitro and in vivo experiments showed that Ang II increased intracellular reactive oxygen species (ROS) production and cardiomyocyte apoptosis; these were reversed by administration of the ROS scavenger N-acetylcysteine and by Mst1 deficiency, which suppressed c-Jun N-terminal kinase (JNK) phosphorylation and downstream signaling. | Reactive Oxygen Species | mitogen-activated protein kinase 8 | Homo sapiens |
| 3 | In vitro and in vivo experiments showed that Ang II increased intracellular reactive oxygen species (ROS) production and cardiomyocyte apoptosis; these were reversed by administration of the ROS scavenger N-acetylcysteine and by Mst1 deficiency, which suppressed c-Jun N-terminal kinase (JNK) phosphorylation and downstream signaling. | Reactive Oxygen Species | mitogen-activated protein kinase 8 | Homo sapiens |
| 4 | Thus, cardiac-specific Mst1 knockout inhibits ROS-mediated JNK signalling to block Ang II-induced cardiomyocyte apoptosis, suggesting Mst1 as a potential therapeutic target for treatment of RAAS-activated heart failure. | Reactive Oxygen Species | mitogen-activated protein kinase 8 | Homo sapiens |