Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.1.1.8 (
cholinesterase
)
12,691
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Coagulation factor XIII
is a transglutaminase catalysing the crosslinking of fibrin chains as well as the formation of covalent links between several extracellular matrix proteins such as fibronectin, vitronectin and collagen. By mediating the incorporation of alpha2 antiplasmin into the fibrin network, this factor also interferes with fibrinolysis. Increased plasma factor XIII activity was reported by our laboratory 30 years ago in hypertriglyceridemic subjects who also displayed increased activity of serum
cholinesterase
, a marker of hepatic protein synthesis, and a delayed diluted, blood clot lysis time. Recent data in the literature emphasize a relationship between insulin resistance (metabolic syndrome) and increased plasma levels of factor XIII, confirming our results. It was also reported that a faster activation of this factor related to the Val 34 leu polymorphism provides protective effect against myocardial infarction and stroke, this effect being however negated in patients with insulin resistance and high plasma levels of plasminogen activator inhibitor-1. The pathogenic role of factor XIII in atherothrombosis seems to be bivalent. On the one side, an increased activity would favor the persistence of fibrin depositions and increase plaque burden, while on the other side it would reduce plaque vulnerability and the risk of downstream embolization.
...
PMID:Coagulation factor XIII and atherothrombosis. A mini-review. 1552 18
Studies initiated 30 years ago emphasized that dilute blood clot lysis time was longer in obese diabetic patients than in normal weight diabetics. It was also later reported that when compared to obese women with gluteal and femoral adiposity, the age matched men with abdominal obesity displayed a more delayed clot lysis, higher triglyceride levels and higher
cholinesterase
activity, as well as more increased concentration of plasminogen activator inhibitor-1 (PAL-1). According to authors' investigations and data in the literature, impaired fibrinolysis in overweight hypertriglyceridemic subjects are mainly due to increased plasma levels of
coagulation factor XIII
and PAI-1. It could also be demonstrated that plasma clotting factors VII and VIII activities as well as plasma fibrinogen and von Willebrand factor levels were higher in patients with type 2 diabetes and abdominal obesity than in diabetics without obesity. Such findings are supporting data in the literature, insisting on the pathogenic relevance of intraabdominal obesity and of the subsequently enhanced release of fatty acids and of proinflammatory cytokines in the portal flow. Surprisingly anticoagulant plasma proteins C and S levels were found to be increased in overweight and hyperlipidemic patients considered to be at risk for thrombotic complications. Recent data in the literature had however demonstrated that circulating protein C zymogen acquires anticoagulant activity only after its binding to specific receptors on endothelial cell membrane, while proinflammatory cytokines may disrupt this activating interaction with vascular endothelia.
...
PMID:Thrombotic tendency in diabetes mellitus. Revisiting and revising a study initiated 30 years ago. 2332 54