H₂S protects against pressure overload-induced heart failure via upregulation of endothelial nitric oxide synthase.

ABSTRACT:

Background

Cystathionine γ-lyase (CSE) produces H2S via enzymatic conversion of L-cysteine and plays a critical role in cardiovascular homeostasis. We investigated the effects of genetic modulation of CSE and exogenous H2S therapy in the setting of pressure overload-induced heart failure.

Methods and results

Transverse aortic constriction was performed in wild-type, CSE knockout, and cardiac-specific CSE transgenic mice. In addition, C57BL/6J or CSE knockout mice received a novel H2S donor (SG-1002). Mice were followed up for 12 weeks with echocardiography. We observed a >60% reduction in myocardial and circulating H2S levels after transverse aortic constriction. CSE knockout mice exhibited significantly greater cardiac dilatation and dysfunction than wild-type mice after tr

SUBMITTER: Kondo K 

PROVIDER: S-EPMC3670187 | biostudies-literature | 2013 Mar

REPOSITORIES: biostudies-literature