Published online Feb 15, 2015. doi: 10.4239/wjd.v6.i1.54
Peer-review started: July 2, 2014
First decision: September 18, 2014
Revised: November 20, 2014
Accepted: December 3, 2014
Article in press: December 10, 2014
Published online: February 15, 2015
Diabetes mellitus is one of the most potent independent risk factors for the development of diabetic cerebral vascular disease (CVD). Many evidences suggested that hyperglycemia caused excess free fatty acids, the loss of endothelium-derived nitric oxide, insulin resistance, the prothrombotic state, endothelial dysfunction, the abnormal release of endothelial vasoactivators, vascular smooth muscle dysfunction, oxidative stress, and the downregulation of miRs participated in vessel generation and recovery as well as the balance of endotheliocytes. In turn, these abnormalities, mainly via phosphatidylinositol 3 kinase, mitogen-activated protein kinase, polyol, hexosamine, protein kinase C activation, and increased generation of advanced glycosylation end products pathway, play an important role in inducing diabetic CVD complication. A deeper comprehension of pathogenesis producing diabetic CVD could offer base for developing new therapeutic ways preventing diabetic CVD complications, therefore, in the paper we mainly reviewed present information about the possible pathogenesis of diabetic CVD complication.
Core tip: A better understanding pathogenesis of diabetic cerebral vascular disease (CVD) could provide the basis for developing novel therapeutic strategies against diabetic CVD complication. Our article highlights the pathogenesis as some promising options to prevent CVD complications in diabetes, including metabolic and vascular changes and main pathways are involved in diabetic CVD complication.