Xiangru Lu

Early and persistent activation of myocardial apoptosis, bax and caspases: insights into mechanisms of progression of heart failure.

Development of heart failure and congenital septal defects in mice lacking endothelial nitric oxide synthase.

Deficiency in endothelial nitric oxide synthase impairs myocardial angiogenesis.

Endothelial nitric-oxide synthase enhances lipopolysaccharide-stimulated tumor necrosis factor-alpha expression via cAMP-mediated p38 MAPK pathway in cardiomyocytes.

Inhibition of p38 MAPK decreases myocardial TNF-alpha expression and improves myocardial function and survival in endotoxemia.

Upregulation of corin gene expression in hypertrophic cardiomyocytes and failing myocardium.

In vivo TNF-alpha inhibition ameliorates cardiac mitochondrial dysfunction, oxidative stress, and apoptosis in experimental heart failure.

Endogenous heme oxygenase induction is a critical mechanism attenuating apoptosis and restoring microvascular perfusion following limb ischemia/reperfusion.

NADH oxidase signaling induces cyclooxygenase-2 expression during lipopolysaccharide stimulation in cardiomyocytes.

Pivotal role of gp91phox-containing NADH oxidase in lipopolysaccharide-induced tumor necrosis factor-alpha expression and myocardial depression.

Fasudil, a Rho-kinase inhibitor, attenuates angiotensin II-induced abdominal aortic aneurysm in apolipoprotein E-deficient mice by inhibiting apoptosis and proteolysis.

Role of tumor necrosis factor-alpha in myocardial dysfunction and apoptosis during hindlimb ischemia and reperfusion.

Lack of endothelial nitric oxide synthase decreases cardiomyocyte proliferation and delays cardiac maturation.

Erythropoietin protects cardiomyocytes from apoptosis via up-regulation of endothelial nitric oxide synthase.

Role of neuronal nitric oxide synthase in lipopolysaccharide-induced tumor necrosis factor-alpha expression in neonatal mouse cardiomyocytes.

Endothelial nitric oxide synthase promotes neonatal cardiomyocyte proliferation by inhibiting tissue inhibitor of metalloproteinase-3 expression.

Longitudinal follow-up of cardiac structure and functional changes in an infarct mouse model using retrospectively gated micro-computed tomography.

Role of heme oxygenase-1 in the cardioprotective effects of erythropoietin during myocardial ischemia and reperfusion.

JNK1/c-fos inhibits cardiomyocyte TNF-alpha expression via a negative crosstalk with ERK and p38 MAPK in endotoxaemia.

Tissue inhibitor of metalloproteinase-3 inhibits neonatal mouse cardiomyocyte proliferation via EGFR/JNK/SP-1 signaling.

Endothelial nitric oxide synthase promotes bone marrow stromal cell migration to the ischemic myocardium via upregulation of stromal cell-derived factor-1alpha.

Cardiomyocyte-specific overexpression of human stem cell factor improves cardiac function and survival after myocardial infarction in mice.

Neuronal nitric oxide synthase protects against myocardial infarction-induced ventricular arrhythmia and mortality in mice.

Effects of anemia and blood transfusion in acute myocardial infarction in rats.

Comparison of initial cell retention and clearance kinetics after subendocardial or subepicardial injections of endothelial progenitor cells in a canine myocardial infarction model.

Rac1 activation induces tumour necrosis factor-α expression and cardiac dysfunction in endotoxemia.

NOX2 deficiency protects against streptozotocin-induced beta-cell destruction and development of diabetes in mice.

Erythropoietin is equally effective as fresh-blood transfusion at reducing infarct size in anemic rats.

Deficiency in TIMP-3 increases cardiac rupture and mortality post-myocardial infarction via EGFR signaling: beneficial effects of cetuximab.

North American ginseng protects the heart from ischemia and reperfusion injury via upregulation of endothelial nitric oxide synthase.

Transfusion of fresh but not old stored blood reduces infarct size and improves cardiac function after acute myocardial infarction in anemic rats*.

Mitogen-activated protein kinase phosphatase-1 inhibits myocardial TNF-α expression and improves cardiac function during endotoxemia.

Inhibition of Na/K-ATPase promotes myocardial tumor necrosis factor-alpha protein expression and cardiac dysfunction via calcium/mTOR signaling in endotoxemia.

Nitric oxide synthase-3 deficiency results in hypoplastic coronary arteries and postnatal myocardial infarction.

Cardiomyocyte-specific overexpression of human stem cell factor protects against myocardial ischemia and reperfusion injury.

Recombinant human annexin A5 inhibits proinflammatory response and improves cardiac function and survival in mice with endotoxemia.

Nitric oxide synthase-3 promotes embryonic development of atrioventricular valves.

N-Acetylcysteine prevents congenital heart defects induced by pregestational diabetes.

Cardiac-specific overexpression of human stem cell factor promotes epicardial activation and arteriogenesis after myocardial infarction.

Rac1 signaling is critical to cardiomyocyte polarity and embryonic heart development.

Pregestational diabetes induces fetal coronary artery malformation via reactive oxygen species signaling.

Rac1 Signaling Is Required for Anterior Second Heart Field Cellular Organization and Cardiac Outflow Tract Development.

Inhibition of Rac1 reduces store overload-induced calcium release and protects against ventricular arrhythmia.

North American ginseng inhibits myocardial NOX2-ERK1/2 signaling and tumor necrosis factor-α expression in endotoxemia.