Diabetes-induced edothelial dysfuction: Molecular pathways and clinical implication

Endothelial dysfunction caused by diabetic conditions is one of the most pivotal factors in the formation of various CAD. This review will explain the cellular changes in endothelial cells in diabetes mellitus especially hyperglycemia induced damage oxidative stress inflammation and the defects in the eNOS enzyme. High glucose stimulates biomechanisms such as ROS formation, polyol formation, PKC activation, and AGE formation and increased hexosamine formation that are all instrumental in endothelial damage. These mechanisms acting in concert with one another disrupt the normally balanced endothelial function contributing to reduction in bioavailability of nitric oxide (NO), increased permeability of the endothelium and pro-inflammatory and pro-thrombotic states. Chronic inflammations exacerbate endothelial dysfunction because of the sustained release of ROS and the production of apoptotic signals in endothelial cells. Furthermore, the review also consider’s the roles of microRNAs and epigenomics in managing diabetic endothelial nations. Endothelial dysfunction in a clinical perspective is a leading factor to atherosclerosis, hypertension as well as other vascular complications that affect diabetic patients. Therapeutic approaches in regard to endothelial dysfunction: non-pharmacological interventions, drug interventions (statins; ACE inhibitors; SGLT2 inhibitors; GLP-1 receptor agonists, etc.). From this review, it can be concluded that screening for and more particularly tackling endothelial dysfunction is crucial during the early stages of diabetes to minimize cardiovascular risks and translate into better patient outcomes. It is crucial to have a better comprehension of these molecular cascades to advance novel treatment approaches consistent with the preservation of endothelial integrity in diabetes and its comparatively worse vascular complications.