Authors: Yonghe Ding, Xiaojing Sun and Xiaolei Xu

Yonghe Ding

Department of Biochemistry and Molecular Biology/Division of Cardiovascular Diseases; Department of Medicine; Mayo Clinic College of Medicine; Rochester, MN USA

Xiaojing Sun

Department of Biochemistry and Molecular Biology/Division of Cardiovascular Diseases; Department of Medicine; Mayo Clinic College of Medicine; Rochester, MN USA

Xiaolei Xu

Corresponding author: xu.xiaolei@mayo.edu
Department of Biochemistry and Molecular Biology/Division of Cardiovascular Diseases; Department of Medicine; Mayo Clinic College of Medicine; Rochester, MN USA

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.

Autophagic Punctum to:
Y Ding, X Sun, W Huang, T Hoage, M Redfield, S Kushwaha, S Sivasubbu, X Lin, S Ekker, X Xu. Haploinsufficiency of target of rapamycin attenuates cardiomyopathies in adult zebrafish. Circ Res 2011; 109: 658-69
PMID: 21757652 DOI: 10.1161/CIRCRESAHA.111.248260