“…Its biological role is probably based on its binding capacities; it binds to plasminogen kringle 4 domain and to ASTK1-4, enhancing plasminogen activation by tissue-type plasminogen activator and partially counteracting the ability of ASTK1-4 to inhibit the proliferation of endothelial cells (13). Decreased plasma TN levels were found in patients with CAD with gradually lower values from stable to unstable angina until acute myocardial infarction, and therapeutic treatment with rtPA has resulted in an increase of plasma TN levels (24,25). The difference of TN response to CPB postoperatively compared with the biphasic alteration of sP-s could be due to the fact that plasma TN levels are strictly regulated depending on TN release by cells, TN bound in fibrin or other molecules, and TN excretion from the body.…”
CPB is characterised by pronounced changes in plasma sP-s, sE-s, TN, vWF levels, and ACE activity, which are associated with significant alteration in the intra- and early postoperative endothelial function observed in open heart surgery.
“…Its biological role is probably based on its binding capacities; it binds to plasminogen kringle 4 domain and to ASTK1-4, enhancing plasminogen activation by tissue-type plasminogen activator and partially counteracting the ability of ASTK1-4 to inhibit the proliferation of endothelial cells (13). Decreased plasma TN levels were found in patients with CAD with gradually lower values from stable to unstable angina until acute myocardial infarction, and therapeutic treatment with rtPA has resulted in an increase of plasma TN levels (24,25). The difference of TN response to CPB postoperatively compared with the biphasic alteration of sP-s could be due to the fact that plasma TN levels are strictly regulated depending on TN release by cells, TN bound in fibrin or other molecules, and TN excretion from the body.…”
CPB is characterised by pronounced changes in plasma sP-s, sE-s, TN, vWF levels, and ACE activity, which are associated with significant alteration in the intra- and early postoperative endothelial function observed in open heart surgery.
“…While TN is not found in the ECM of normal tissue, it has been found in abundance in that of malignant tumours, where it serves as an anchorage and reservoir of plasminogen, promoting tumour growth and metastasis. Its plasma levels are approximately 100 n m in healthy adults (36), while it was found clearly reduced in patients with cancer, rheumatoid arthritis, coronary disease but increased in T1DM patients (36–40). The mechanisms through which TN may participate in the development of such diseases are under investigation.…”
Decreased antioxidative protection from simultaneous LPO and NOx overproduction is evident in T1DM juveniles with a parallel endothelial/platelet activation even in the first years of the disease, being more pronounced later in diabetes progression, contributing to the vascular complications of the disease.
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