Abstract
The target of rapamycin (TOR) kinase is part of an evolutionarily conserved signaling pathway that coordinates cell growth, survival, and autophagy. Previously, pharmacological studies using rapamycin have suggested a cardioprotective effect of TOR signaling inhibition on cardiomyopathy. We found that rapamycin exerts a conserved cardioprotective effect in two adult zebrafish models of cardiomyopathy of different etiology, and provided the first genetic evidence to support a long-term cardioprotective effect of TOR signaling inhibition. Moreover, we detected dynamic TOR-autophagy activities along different stages of cardiomyopathy. This needs to be considered when developing TOR-autophagy-based therapeutics for cardiomyopathy.
Original language | English (US) |
---|---|
Pages (from-to) | 142-143 |
Number of pages | 2 |
Journal | Autophagy |
Volume | 8 |
Issue number | 1 |
DOIs | |
State | Published - Jan 2012 |
Keywords
- Anemia
- Autophagy
- Cardiomyopathy
- Cardioprotective
- Doxorubicin
- Target of rapamycin
- Zebrafish
ASJC Scopus subject areas
- Molecular Biology
- Cell Biology