Myeloperoxidase and plasminogen activator inhibitor 1 play a central role in ventricular remodeling after myocardial infarction. - Test2 - elhamkhani - TriplyDB

Myeloperoxidase and plasminogen activator inhibitor 1 play a central role in ventricular remodeling after myocardial infarction.

Myeloperoxidase and plasminogen activator inhibitor 1 play a central role in ventricular remodeling after myocardial infarction.

http://www.wikidata.org/entity/Q36370540

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Cathepsin g is required for sustained inflammation and tissue injury after reperfusion of ischemic kidneys Increased systemic and myocardial expression of neutrophil gelatinase-associated lipocalin in clinical and experimental heart failure Plasminogen activator inhibitor-1 (PAI-1) is cardioprotective in mice by maintaining microvascular integrity and cardiac architecture.Elevated plasma free fatty acids increase cardiovascular risk by inducing plasma biomarkers of endothelial activation, myeloperoxidase and PAI-1 in healthy subjects Pleiotropic functions of plasminogen activator inhibitor-1.Olmesartan prevents cardiac rupture in mice with myocardial infarction by modulating growth differentiation factor 15 and p53 Association between peak neutrophil count, clopidogrel loading dose, and left ventricular systolic function in patients with primary percutaneous coronary intervention.Role of vegetation-associated protease activity in valve destruction in human infective endocarditis.Comprehensive peroxidase-based hematologic profiling for the prediction of 1-year myocardial infarction and death.Role of biomarkers in risk stratification of acute coronary syndrome Increased expression of plasminogen activator inhibitor-1 in cardiomyocytes contributes to cardiac fibrosis after myocardial infarction.Differential regenerative capacity of neonatal mouse hearts after cryoinjury.Reactive oxygen species in cardiovascular disease.Matricellular proteins in cardiac adaptation and disease.Role of oxidative stress in disease progression in Stage B, a pre-cursor of heart failure.Early postmyocardial infarction survival in Murphy Roths Large mice is mediated by attenuated apoptosis and inflammation but depends on genetic background Detection and quantification of fluorescent cell clusters in cryo-imaging.Fibrosis in Atrial Fibrillation - Role of Reactive Species and MPO.Arjunolic acid ameliorates reactive oxygen species via inhibition of p47(phox)-serine phosphorylation and mitochondrial dysfunction Periostin is essential for cardiac healing after acute myocardial infarction.Matrix metalloproteinase-28 deletion exacerbates cardiac dysfunction and rupture after myocardial infarction in mice by inhibiting M2 macrophage activation.Identification of nondiabetic heart failure-associated genes by bioinformatics approaches in patients with dilated ischemic cardiomyopathy.Validation of the vitronectin knockout mouse as a model for studying myocardial infarction: Vitronectin appears to influence left ventricular remodelling following myocardial infarction.Atrial natriuretic peptide increases inflammation, infarct size, and mortality after experimental coronary occlusion.Genetic enhancement of stem cell engraftment, survival, and efficacy.Usefulness of myeloperoxidase levels in healthy elderly subjects to predict risk of developing heart failure.Potential novel pharmacological therapies for myocardial remodelling.Myeloperoxidase, modified lipoproteins, and atherogenesis.Modification of high density lipoprotein by myeloperoxidase generates a pro-inflammatory particle.Naoxintong attenuates Ischaemia/reperfusion Injury through inhibiting NLRP3 inflammasome activation.Evaluation of serum myeloperoxidase concentration in dogs with heart failure due to chronic mitral valvular insufficiency.Current role of myeloperoxidase in routine clinical practice.Risk stratification and short-term prognosis in acute heart failure syndromes: a review of novel biomarkers.Mitochondrial mitophagic mechanisms of myocardial matrix metabolism and remodelling.Neutrophil roles in left ventricular remodeling following myocardial infarction.Molecular imaging of macrophage enzyme activity in cardiac inflammation.Loss or inhibition of uPA or MMP-9 attenuates LV remodeling and dysfunction after acute pressure overload in mice.The Time Course of Markers of Neutrophil Extracellular Traps in Patients Undergoing Revascularisation for Acute Myocardial Infarction or Stable Angina Pectoris.Apolipoprotein A1 regulates coenzyme Q10 absorption, mitochondrial function, and infarct size in a mouse model of myocardial infarction.Myeloperoxidase is critically involved in the induction of organ damage after renal ischemia reperfusion.

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Myeloperoxidase and plasminogen activator inhibitor 1 play a central role in ventricular remodeling after myocardial infarction.

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Myeloperoxidase and plasminoge ...... g after myocardial infarction.

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Myeloperoxidase and plasminoge ...... g after myocardial infarction.

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Myeloperoxidase and plasminoge ...... g after myocardial infarction.

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Myeloperoxidase and plasminoge ...... g after myocardial infarction.

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Myeloperoxidase and plasminoge ...... g after myocardial infarction.

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Annitta Morehead

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Arman T Askari

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James D Thomas

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Jeanne Drinko

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Marc S Penn

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Marie-Luise Brennan

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Stanley L Hazen

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Xiaorong Zhou

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P2860

Protein measurement with the Folin phenol reagent

Human plasminogen activator inhibitor-1 (PAI-1) deficiency: characterization of a large kindred with a null mutation in the PAI-1 gene

Studies on the chlorinating activity of myeloperoxidase

Increased atherosclerosis in myeloperoxidase-deficient mice

Endothelial transcytosis of myeloperoxidase confers specificity to vascular ECM proteins as targets of tyrosine nitration

Colocalization of thrombin, PAI-1, and vitronectin in the atherosclerotic vessel wall: A potential regulatory mechanism of thrombin activity by PAI-1/vitronectin complexes

The oxidative inactivation of plasminogen activator inhibitor type 1 results from a conformational change in the molecule and does not require the involvement of the P1' methionine.

Influence of prior ACE inhibitor therapy on morbidity and mortality following acute myocardial infarction.

Oxidative stress regulates collagen synthesis and matrix metalloproteinase activity in cardiac fibroblasts.

Plasminogen activator inhibitor-1 gene-deficient mice. I. Generation by homologous recombination and characterization.

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12615902

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