Introduction:
Diabetes Mellitus (DM) acts as an absolute mediator of cardiovascular risk,
prompting the prolonged occurrence, size and intricacy of atherosclerotic plaques via enhanced Advanced
Glycation Endproducts (AGEs) formation. Moreover, hyperglycemia is associated with enhanced
glyco-oxidized and oxidized Low-Density Lipoprotein (LDL) possessing greater atherogenicity
and decreased the ability to regulate HMG-CoA reductase (HMG-R). Although aminoguanidine (AG)
prevents the AGE-induced protein cross-linking due to its anti-glycation potential, it exerts several unusual
pharmaco-toxicological effects thus restraining its desirable therapeutic effects. HMG-R inhibitors/statins exhibit a variety of beneficial impacts in addition to the cholesterol-lowering effects.
Objective:
Inhibition of AGEs interaction with receptor for AGEs (RAGE) and glyco-oxidized-LDL by
HMG-R inhibitors could decrease LDL uptake by LDL-receptor (LDL-R), regulate cholesterol synthesis
via HMG-R, decrease oxidative and inflammatory stress to improve the diabetes-associated
complications.
Conclusion:
Current article appraises the pathological AGE-RAGE concerns in diabetes and its associated
complications, mainly focusing on the phenomenon of both circulatory AGEs and those accumulating
in tissues in diabetic nephropathy, diabetic neuropathy, and diabetic retinopathy, discussing the
potential protective role of HMG-R inhibitors against diabetic complications.
Effect of lectin-like oxidized LDL receptor-1 polymorphism on liver disease, glucose homeostasis, and postprandial lipoprotein metabolism in nonalcoholic steatohepatitis