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[Plasminogen activator inhibitor (PAI-1) and diabetes mellitus. I. Regulation of PAI-1 levels].

Authors: P, Galajda; L, Sutarík; L, Vladár; J, Stasko; P, Kubisz; M, Mokán;

[Plasminogen activator inhibitor (PAI-1) and diabetes mellitus. I. Regulation of PAI-1 levels].

Abstract

Elevated PAI-1 levels were described in different insulin resistant conditions, incl. diabetes mellitus type II. In its formation probably several stimulating factors participate. Hitherto accomplished studies suggest not only the important effect of insulin acting synergically with very low density. lipoproteins (VLDL) on hepatocytes but also the importance of the endothelial pool where the action of proinsulin, VLDL and cytokines in synergy with Cai-dependent stimuli (oxidation stress, thrombin) is involved. Under certain circumstances also another adipocyte compartment may play a role, and a significant role of thrombocytes in raising the PAI-1 level cannot be ruled out either. A more detailed analysis of the raised PAI-1 level in different patients could extend the possibilities of therapeutic reduction of levels of this important risk factor of atherosclerosis.

Keywords

Diabetes Mellitus, Type 2, Plasminogen Activator Inhibitor 1, Humans

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selected citations
These citations are derived from selected sources.
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
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Average
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