Abstract
Diabetes is considered a major risk factor for stroke and is associated with worsened stroke outcomes. Here, we discuss and summarize the mechanisms that have been associated with the increased risk of stroke due to the hyperglycemia in diabetes mellitus. In diabetic stroke models, hyperglycemia exaggerates the following damaging processes: acidosis, accumulation of reactive oxygen species/reactive nitrogen, inflammation and mitochondrial dysfunction. Understanding the mechanism of diabetes acting as a stroke risk factor will definitely assist to reveal issues related to drug metabolism and toxicity in diabetic stroke. In addition, it is suggested that future studies may focus on the mechanisms mediating blood-brain barrier and astrocytes dysfunction under hyperglycemic stroke.
Highlights
According to the World Health Organization, over 15 million people, equating to one in every 400 people, suffer a stroke worldwide a year [1]
This review aims to discuss and summarize the mechanisms that have been associated with the increased risk of stroke due to the hyperglycemia in diabetes mellitus
According to a variety of findings in the literature, four main pathways, including acidosis, reactive oxygen species/reactive nitrogen species, inflammation, and mitochondrial dysfunction are involved in hyperglycemia-aggravated stroke
Summary
According to the World Health Organization, over 15 million people, equating to one in every 400 people, suffer a stroke worldwide a year [1]. High glucose levels result in increased nitric oxide and superoxide production, leading to peroxynitrite formation [37,38,39] Given both ischemia and hyperglycemia induces the formation of peroxynitrite, the peroxynitrite level in diabetic stroke was much higher than non-diabetic stroke [30]. Lin et al demonstrated that hyperglycemia triggered early, massive deposition of neutrophils in the post-ischemic brain, which might exacerbate injury [47] This increased adhesion of leukocytes to the endothelial cells was largely due to the increased expression of cell adhesion molecules on endothelial cells. The elevation of HMGB1 during hyperglycemic ischemia may contribute to inflammatory response
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