Endothelial and platelet dysfunction play a key role in the pathogenesis of diabetic angiopathy, highlighting potential therapeutic targets.
Answers are grounded in this paper and cite their sources.
May highlight therapeutic targets in diabetic angiopathy; leaves open confirmation in randomized trials.
The deterioration of the circulation in small and large vessels in diabetes seems to be related to abnormalities of the function of the endothelial cells and of the platelets. The endothelial factor VIII R:Ag, enhancing platelet adhesion, is increased, while fibrinolysis is decreased. The balance between thromboxane (platelet-aggregating) and prostacyclin (desaggregating) is also shifted in a similar way. These changes all favour increased deposition and delayed removal of platelets and fibrin on the intima, and they might contribute markedly to the development of diabetic angiopathy. Some new drugs seem to normalize the endothelial fibrinolytic activity, and long term studies are in progress to evaluate if this improvement is parallelled by a delayed or absent development of vascular complications.
No takes yet. Share an insight, caveat, or question.
L.‐O. Almér (1982) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: