NFAT and Hypertrophy of the heart (Transcription in the broken heart)
| PAG Title | NFAT and Hypertrophy of the heart (Transcription in the broken heart) |
| PAG ID | WIG000385 |
| Type | P |
| Source Link |  MSigDB |
| Publication Reference | NA |
| PAG Description | Hypertrophy associated with both hypertension and obstruction to ventricular outflow leads to pathologic cardiac growth and it is associated with increase morbidity and mortality. Symptomatic ventricular disease takes a growing toll on the health of nations. As other cardiovascular diseases such as stroke and myocardial infraction are in decline as causes of mortality, the heart failure problem becomes increasingly urgent. Congenital heart defects occur in 1% of live births and fetal heart malformations are implicated in many pregnancies that end in still-birth or spontaneous abortion. The current paradigm suggests that the heart adapts to excess of hemodynamic loading by compensatory hypertrophy, which under condition of persistent stress, over time evolves into dysfunction and myocardial failure. There is considerable evidence that direct effects of increased mechanical stress are sensed within the ventricular wall and that signals critical for the generation of growth responses. Despite compelling statistics we still do not understand biochemically why heart defects are so prevalent. A single transcriptional regulator initially associated with the activation of the T-cells |
| Species | Homo sapiens |
| Quality Metric Scores | nCoCo Score: 1,634 |
| Information Content | Rich |
| Other IDs | M2288 |
| Base PAG ID | WIG000385 |
| Human Phenotyte Annotation | |
| Curator | PAGER curation team |
| Curator Contact | PAGER-contact@googlegroups.com |
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