Circulating NOS3 modulates left ventricular remodeling following reperfused myocardial infarction

Nitric oxide (NO) is constitutively produced and released from the endothelium and several blood cell types by the isoform 3 of the NO synthase (NOS3). We have shown that NO protects against myocardial ischemia/reperfusion (I/R) injury and that depletion of circulating NOS3 increases within 24 h of...

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Veröffentlicht in:	PloS one 2015-04, Vol.10 (4), p.e0120961-e0120961
Hauptverfasser:	Gorressen, Simone, Stern, Manuel, van de Sandt, Annette M, Cortese-Krott, Miriam M, Ohlig, Jan, Rassaf, Tienush, Gödecke, Axel, Fischer, Jens W, Heusch, Gerd, Merx, Marc W, Kelm, Malte
Format:	Artikel
Sprache:	eng
Schlagworte:	Analysis Animals Blood Blood cells Bone marrow Bone marrow transplantation Cardiology Catheters Cicatrix - metabolism Cicatrix - pathology Collagen Collagen (type I) Collagen - analysis Depletion Echocardiography Endothelium Extracellular matrix Fibrosis Gene expression Heart Heart attack Heart attacks Heart failure Hemodynamics Hostages Ischemia Male Medical instruments Medicine Mice Mice, Inbred C57BL Mice, Knockout Myocardial infarction Myocardial Infarction - enzymology Myocardial Infarction - pathology Myocardial ischemia Myocardial Reperfusion Injury - enzymology Myocardial Reperfusion Injury - pathology Nitric oxide Nitric Oxide - physiology Nitric Oxide Synthase Type III - blood Nitric Oxide Synthase Type III - deficiency Nitric Oxide Synthase Type III - genetics Nitric Oxide Synthase Type III - physiology Nitric-oxide synthase Occlusion Polymerase chain reaction Pressure Radiation Chimera Reperfusion Rodents Stem cell transplantation Stroke Volume Structure-function relationships Ventricle Ventricular Dysfunction, Left - enzymology Ventricular Dysfunction, Left - etiology Ventricular Dysfunction, Left - physiopathology Ventricular Remodeling - physiology
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