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pyrophosphatase/infarci
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CD73 on T Cells Orchestrates Cardiac Wound Healing After Myocardial Infarction by Purinergic Metabolic Reprogramming.
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BACKGROUND
T cells are required for proper healing after myocardial infarction. The mechanism of their beneficial action, however, is unknown. The proinflammatory danger signal ATP, released from damaged cells, is degraded by the ectonucleotidases CD39 and CD73 to the anti-inflammatory mediator
Role of pyrophosphate in vascular calcification in chronic kidney disease.
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Vascular calcification is a pathology characterized by the deposition of calcium-phosphate in cardiovascular structures, mainly in the form of hydroxyapatite crystals, resulting in ectopic calcification. It is correlated with increased risk of cardiovascular disease and myocardial infarction in
Hypophosphatemic rickets developed after treatment with etidronate disodium in a patient with generalized arterial calcification in infancy.
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Ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1) was originally reported as a responsible gene for generalized arterial calcification in infancy (GACI). Though the prognosis of GACI patients is poor because of myocardial infarction and heart failure in relation to medial calcification of
The K121Q polymorphism of ENPP1 and peripheral arterial disease.
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The K121Q variant of the ectonucleotide pyrophosphatase/ phosphodiesterase 1 (ENPP1) gene is associated with obesity, insulin resistance, and early myocardial infarction. Therefore, we hypothesized that the K121Q polymorphism might also be associated with an increased risk for peripheral arterial
[ENPP1 K121Q polymorphism and ischemic heart disease in diabetic patients].
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BACKGROUND
The ecto-nucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1) gene is a candidate gene for insulin resistance. Insulin resistance is a major component of metabolic syndrome (MetS) and has been implicated in ischemic heart disease (IHD).
OBJECTIVE
To evaluate the association between the
[Aminoacyl-tRNA-synthetases and their high molecular weight complexes in experimental myocardial ischemia].
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A number of aminoacyl-tRNA synthetases from rabbit liver during experimental myocardial infarction and from pig myocardium upon 15-min of autolysis were found to increase their activity in aminoacylation. Direct correlations between the activities of high molecular weight complexes and of the total
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