Emmanuel S. Buys

MyD88 and NOS2 are essential for toll-like receptor 4-mediated survival effect in cardiomyocytes.

Tissue Doppler imaging predicts left ventricular dysfunction and mortality in a murine model of cardiac injury.

Cardiomyocyte-specific overexpression of nitric oxide synthase 3 prevents myocardial dysfunction in murine models of septic shock.

Cardiomyocyte-restricted restoration of nitric oxide synthase 3 attenuates left ventricular remodeling after chronic pressure overload.

Disruption of nitric oxide synthase 3 protects against the cardiac injury, dysfunction, and mortality induced by doxorubicin.

Congenital NOS2 deficiency prevents impairment of hypoxic pulmonary vasoconstriction in murine ventilator-induced lung injury.

Inhaled agonists of soluble guanylate cyclase induce selective pulmonary vasodilation.

Gender-specific hypertension and responsiveness to nitric oxide in sGCalpha1 knockout mice.

Innate immune adaptor MyD88 mediates neutrophil recruitment and myocardial injury after ischemia-reperfusion in mice.

A short duration of high-fat diet induces insulin resistance and predisposes to adverse left ventricular remodeling after pressure overload.

Protective effects of nitric oxide synthase 3 and soluble guanylate cyclase on the outcome of cardiac arrest and cardiopulmonary resuscitation in mice.

Small intestinal motility in soluble guanylate cyclase alpha1 knockout mice: (Jejunal phenotyping of sGCalpha1 knockout mice).

sGC(alpha)1(beta)1 attenuates cardiac dysfunction and mortality in murine inflammatory shock models.

Nitrite protects against morbidity and mortality associated with TNF- or LPS-induced shock in a soluble guanylate cyclase-dependent manner.

Nos3 protects against systemic inflammation and myocardial dysfunction in murine polymicrobial sepsis.

Soluble guanylate cyclase alpha1beta1 limits stroke size and attenuates neurological injury.

Soluble guanylate cyclase-α1 is required for the cardioprotective effects of inhaled nitric oxide.

Toll-like receptor 4 signaling confers cardiac protection against ischemic injury via inducible nitric oxide synthase- and soluble guanylate cyclase-dependent mechanisms.

sGC{alpha}1 mediates the negative inotropic effects of NO in cardiac myocytes independent of changes in calcium handling.

Nitric oxide regulates pulmonary vascular smooth muscle cell expression of the inducible cAMP early repressor gene.

Inhaled nitric oxide improves outcomes after successful cardiopulmonary resuscitation in mice.

Genetic modifiers of hypertension in soluble guanylate cyclase α1-deficient mice.

In vivo noninvasive characterization of brown adipose tissue blood flow by contrast ultrasound in mice.

Pathophysiology of hypertension in the absence of nitric oxide/cyclic GMP signaling.

Soluble guanylate cyclase α1-deficient mice: a novel murine model for primary open angle glaucoma.