Prostanoids and thromboxane A2 involvement in diabetic retinopathy.
Alteration in prostanoid and TXA2 production are involved in the development of diabetic microangiopathy underlying DR. Diabetic microangiopathy is characterized by abnormalities in platelet function and increased susceptibility to thrombus formation. The synthesis of excessive amounts of PGs and TXA2 by platelets obtained from diabetic patients is underlying alteration in platelet responsiveness seen in diabetes mellitus. An associated reduction in PGI2 by endothelial blood vessels results in further disruption of the homeostatic mechanism regulating the aggregatory process. However, PGI2 behaviour in different tissues, and in blood vessels of varied calibre is yet unclear. PGI2 synthesis is restored to normal on reduction of blood glucose levels. Restoration of the synthesis of both prostanoids and PGI2 to normal, might be achieved by using drugs that inhibit prostanoid and TXA2 formation as well as by controlling glucose blood levels. Affecting the imbalance of prostanoid and TXA2 seen in diabetes might be of clinical implication in prevention and treatment of DR.
D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism; D003925:Diabetic Angiopathies / Q000209:etiology / Q000378:metabolism; D003930:Diabetic Retinopathy / Q000209:etiology* / Q000378:metabolism; D015232:Dinoprostone; D011464:Epoprostenol / Q000096:biosynthesis; D006706:Homeostasis; D006801:Humans; D011453:Prostaglandins / Q000502:physiology*; D011458:Prostaglandins E / Q000096:biosynthesis; D051381:Rats; D011919:Rats, Inbred Strains; D012160:Retina / Q000378:metabolism; D013928:Thromboxane A2 / Q000502:physiology*; D013931:Thromboxanes / Q000502:physiology*
D011453:Prostaglandins; D011458:Prostaglandins E; D013931:Thromboxanes; D013928:Thromboxane A2; D011464:Epoprostenol; D015232:Dinoprostone