Abstract
Background - Calcineurin (CnA) is important in the regulation of myocardial hypertrophy. We demonstrated that targeted proteolysis of the CnA autoinhibitory domain under pathological myocardial workload leads to increased CnA activity in human myocardium. Here, we investigated the proteolytic mechanism leading to activation of CnA. Methods and Results - In patients with diseased myocardium, we found strong nuclear translocation of CnA. In contrast, in normal human myocardium, there was a cytosolic distribution of CnA. Stimulation of rat cardiomyocytes with angiotensin (Ang) II increased calpain activity significantly (433±11%; P
Original language | English |
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Pages (from-to) | 1045-1053 |
Number of pages | 8 |
Journal | Circulation |
Volume | 111 |
Issue number | 8 |
DOIs | |
Publication status | Published - 1 Mar 2005 |
Keywords
- Calcium
- Hypertrophy
- Molecular biology
- Myocardium