Please use this identifier to cite or link to this item: https://doi.org/10.1038/ng.129
Title: Soluble epoxide hydrolase is a susceptibility factor for heart failure in a rat model of human disease
Authors: Monti J.
Fischer J.
Paskas S.
Heinig M.
Schulz H.
G�sele C.
Heuser A.
Fischer R.
Schmidt C.
Schirdewan A.
Gross V.
Hummel O.
Maatz H.
Patone G.
Saar K.
Vingron M.
Weldon S.M.
Lindpaintner K.
Hammock B.D.
Rohde K.
Dietz R.
Cook S.A. 
Schunck W.-H.
Luft F.C.
Hubner N.
Issue Date: 2008
Publisher: Nature Research
Citation: Monti J., Fischer J., Paskas S., Heinig M., Schulz H., G�sele C., Heuser A., Fischer R., Schmidt C., Schirdewan A., Gross V., Hummel O., Maatz H., Patone G., Saar K., Vingron M., Weldon S.M., Lindpaintner K., Hammock B.D., Rohde K., Dietz R., Cook S.A., Schunck W.-H., Luft F.C., Hubner N. (2008). Soluble epoxide hydrolase is a susceptibility factor for heart failure in a rat model of human disease. Nature Genetics 40 (5) : 529-537. ScholarBank@NUS Repository. https://doi.org/10.1038/ng.129
Abstract: We aimed to identify genetic variants associated with heart failure by using a rat model of the human disease. We performed invasive cardiac hemodynamic measurements in F2 crosses between spontaneously hypertensive heart failure (SHHF) rats and reference strains. We combined linkage analyses with genome-wide expression profiling and identified Ephx2 as a heart failure susceptibility gene in SHHF rats. Specifically, we found that cis variation at Ephx2 segregated with heart failure and with increased transcript expression, protein expression and enzyme activity, leading to a more rapid hydrolysis of cardioprotective epoxyeicosatrienoic acids. To confirm our results, we tested the role of Ephx2 in heart failure using knockout mice. Ephx2 gene ablation protected from pressure overload-induced heart failure and cardiac arrhythmias. We further demonstrated differential regulation of EPHX2 in human heart failure, suggesting a cross-species role for Ephx2 in this complex disease. � 2008 Nature Publishing Group.
Source Title: Nature Genetics
URI: http://scholarbank.nus.edu.sg/handle/10635/149996
ISSN: 10614036
DOI: 10.1038/ng.129
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