PUBLICATION
TOR-autophagy signaling in adult zebrafish models of cardiomyopathy
- Authors
- Ding, Y., Sun, X., and Xu, X.
- ID
- ZDB-PUB-120106-6
- Date
- 2012
- Source
- Autophagy 8(1): 142-143 (Journal)
- Registered Authors
- Ding, Yonghe, Sun, Xiaojing, Xu, Xiaolei
- Keywords
- none
- MeSH Terms
-
- Aging/pathology*
- Animals
- Autophagy*
- Cardiomyopathies/enzymology*
- Cardiomyopathies/pathology*
- Cardiotonic Agents/metabolism
- Disease Models, Animal
- Doxorubicin
- Signal Transduction*
- TOR Serine-Threonine Kinases/metabolism*
- Zebrafish/metabolism*
- PubMed
- 22186229 Full text @ Autophagy
Citation
Ding, Y., Sun, X., and Xu, X. (2012) TOR-autophagy signaling in adult zebrafish models of cardiomyopathy. Autophagy. 8(1):142-143.
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.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping