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myocardial infarction/prolina
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Alanine for proline substitution in the peroxisome proliferator-activated receptor gamma-2 (PPARG2) gene and the risk of incident myocardial infarction.
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OBJECTIVE
Recent studies have implicated the potential importance of peroxisome proliferator-activated receptors as a molecular mechanism involved in atherothrombosis. A common alanine (A) for proline (P) substitution at codon 12 in the peroxisome proliferator activated receptor gamma-2 gene
Cardioprotective Effects of Metalloproteinase Inhibitor 1-({4-[(4-Chlorobenzoyl)amino]phenyl}sulfonyl-L-Proline in Modeled Acute Myocardial Infarction.
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Cardioprotective effect of 1-({4 [(4 chlorobenzoyl)amino]phenyl}sulfonyl-L-proline (compound AL-828) was studied in rats with modeled acute myocardial infarction. The test compound was administered intragastrically in a dose of 30 mg/kg/day for 3 days prior to infarction modeling. Metalloproteinase
Proline improves cardiac remodeling following myocardial infarction and attenuates cardiomyocyte apoptosis via redox regulation
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At present, ischemic heart failure (HF) caused by coronary heart disease (CHD) has a high morbidity and mortality, placing a heavy burden on global human health. L-Proline (Pro), a nonessential amino acid and the foundation of proteins in the human body, was found to be protective against oxidative
Therapeutic potential of thymosin-beta4 and its derivative N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) in cardiac healing after infarction.
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Despite the numerous advances made in the prevention and treatment of cardiovascular diseases, there is a need for new strategies to repair and/or regenerate the myocardium after ischemia and infarction in order to prevent maladaptive remodeling and cardiac dysfunction. This article compiles and
Stabilization of hypoxia inducible factor rather than modulation of collagen metabolism improves cardiac function after acute myocardial infarction in rats.
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Prolyl hydroxylase domain-containing enzymes (PHD) hydroxylate a proline residue that controls the degradation of hypoxia inducible factor (HIF). Hypoxia inhibits this hydroxylation thus increasing HIF levels. HIF is upregulated in ischemic tissues, growing tumors and in nonischemic, mechanically
Proline-rich protein is a glycoprotein and an acute phase reactant.
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Proline-rich protein (PRP) is a plasma protein associated with lipoproteins. In an attempt to clarify the biological significance of this protein, we isolated and characterized it and studied the biological role in plasma. PRP was isolated by immunosorber column chromatography and by gel filtration
A new anti-fibrotic drug attenuates cardiac remodeling and systolic dysfunction following experimental myocardial infarction.
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BACKGROUND
Pathological deposition of extracellular matrix in the non-infarct zone (NIZ) of the ventricle post myocardial infarction (MI) is a key contributor to cardiac remodeling and heart failure. FT011, a novel antifibrotic compound, was evaluated for its efficacy in neonatal cardiac fibroblasts
Ac-SDKP reverses inflammation and fibrosis in rats with heart failure after myocardial infarction.
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Inflammation may play an important role in the pathogenesis of cardiac fibrosis in heart failure (HF) after myocardial infarction (MI). N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a naturally occurring antifibrotic peptide whose plasma concentration is increased 4- to 5-fold by
N-acetyl-seryl-aspartyl-lysyl-proline treatment protects heart against excessive myocardial injury and heart failure in mice.
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Myocardial infarction (MI) in mice results in cardiac rupture at 4-7 days after MI, whereas cardiac fibrosis and dysfunction occur later. N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) has anti-inflammatory, anti-fibrotic, and pro-angiogenic properties. We hypothesized that Ac-SDKP reduces
Leucine 7 to proline 7 polymorphism of the preproneuropeptide Y gene is not associated with restenosis after coronary stenting.
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OBJECTIVE
To identify if an association exists between the leucine 7 (Leu7) to proline 7 (Pro7) polymorphism located in the signal peptide of the preproneuropeptide Y (preproNPY) gene and restenosis after coronary stenting. The Pro7 allele of the preproNPY gene affects the plasma levels of human
Serum levels of arginase I are associated with left ventricular function after myocardial infarction.
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Upregulation of arginase redirects the arginine metabolism from nitric oxide (NO) synthesis to the formation of polyamine and proline, thus causing cardiac dysfunction. NO synthesis is also impaired by asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase inhibitor. We
The influence of age on the wound healing of experimental myocardial infarction in rats.
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In 6-weeks-old, 5-months-old and 21-months-old rats myocardial infarction was induced by coronary artery ligature. After performing the ligature the animals were administered 3H-thymidine, 3H-proline or 35S-sulphate at different times. The following parameters were determined: number of DNA- and
The influence of hyperthyroidism and hypothyroidism on the wound healing of experimental myocardial infarction in the rat.
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In hyperthyroid and hypothyroid rats myocardial infarction was produced by coronary artery ligature. At different times following the ligature the animals were given 3H-thymidine or 3H-proline. The following parameters were determined: the number of DNA- and tropocollagen-synthesizing
The influence of diabetes mellitus and hypercorticism on the wound healing of experimental myocardial infarction in rats.
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In diabetic and glucocorticoid-treated rats myocardial infarction is produced by coronary artery ligation. After the ligation was performed the animals were given 3H-thymidine or 3H-proline at different times. The following parameters were determined: number of DNA- and tropocollagen-synthesizing
Platelet membrane collagen receptor glycoprotein VI polymorphism is associated with coronary thrombosis and fatal myocardial infarction in middle-aged men.
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Glycoprotein VI is a platelet collagen receptor binding to subendothelial collagen after a rupture of an atherosclerotic plaque. The GPVI gene is polymorphic with several SNPs and the T13254C polymorphism predicting amino acid substitution (serine to proline) has been associated with the risk of MI
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