The role of diabetes in the onset and development of endothelial dysfunction

Abstract

The vascular endothelium performs many functions. It is a key regulator of vascular homeostasis, maintains a balance between vasodilation and vasoconstriction, inhibition and stimulation of smooth muscle cell migration and proliferation, fibrinolysis and thrombosis, and is involved to regulation of platelet adhesion and aggregation. Endothelial dysfunction (ED) plays the critical role in pathogenesis of diabetes mellitus (DM) vascular complications. The purpose of this review was to consider the mechanisms leading to the occurrence of ED in DM. The paper discusses current literature data concerning the role of hyperglycemia, oxidative stress, advanced glycation end products in endothelial alteration. A separate section is devoted to the particularities of the functioning of the antioxidant system and their significance in the development of ED in DM. The analysis of the literature allows to conclude that pathological activation of glucose utilization pathways causes damage of endothelial cells, which is accompanied by disorders of all their basic functions. Metabolic disorders in DM cause a pronounced imbalance of free radical processes and antioxidant defense, accompanied by oxidative stress of endotheliocytes, which contributes to the progression of ED and the development of vascular complications. Many aspects of multicomponent regulatory reactions in the pathogenesis of the development of ED in DM have not been sufficiently studied.

The role of oxidative stress in diabetes mellitus-induced vascular endothelial dysfunction

“…As a metabolic disease, DM is characterized by chronic hyperglycaemia, hyperlipidaemia, insulin resistance, and hyperinsulinaemia, which cause various complications, including macrovascular and microvascular lesions [ 2 ]. The vascular endothelium, which is a monolayer of flattened endothelial cells on the surface of blood vessels [ 3 ], plays a pivotal role in vascular physiologic function by regulating vascular permeability, cell adhesion, and the migration and proliferation of smooth muscle cells [ 4 ]. Vascular endothelial dysfunction, which is characterized by decreased endothelium-dependent vasodilation, chronic inflammation, hyperpermeability, leukocyte adherence and cell ageing, is the initial stage of vasculopathy and a vital prognostic indicator of diabetic vascular complications [ 5 , 6 ].…”

Cardiometabolic risk factors in patients with type 2 diabetes and sarcopenia

“…В группе с пресаркопенией выявлены значимые атеросклеротические поражения артерий нижних конечностей. АГ и дислипидемия вызывают эндотелиальную дисфункцию сосудов и могут запускать образование атеросклеротических бляшек [32]. При оценке СМАД в работе была зарегистрирована значимая разница по всем стандартным показателям, при этом пациенты с пресаркопенией и СД 2 типа относились к "non-dipper", при наличии пресаркопении отмечали достоверно более высокие значения индекса в состоянии надпорогового АД и вариабельности САД и ДАД за 24 ч. В этой группе при проведении эхокардиографии обнаружены высокие значения массы миокарда по сравнению с пациен-тами, страдающими саркопенией.…”

Effect of liraglutide dose on efficacy of correcting microcirculatory disorders in absolute insulin deficiency of albino rats

“…Chronic hyperglycemia imposes an altering effect on the endothelium, an important mechanism of which is the activation of protein kinase C, which launches multiple intracellular signaling mechanisms that cause an increase in permeability of the vascular wall and disorder of endothelium-dependent vascular dilatation, suppressing the activity of soluble guanylate cyclase, an enzyme, by which nitric oxide (NO) implements its effects, in particular, vasorelaxation [14]. It is worth noting that an important role in the pathogenesis of vascular complications of diabetes mellitus is played by the activation of oxidative stress: an imbalance of prooxidants and antioxidants, leading to the accumulation of highly toxic products of free radical oxidation, which, in turn, leads to the development and progression of endothelial dysfunction [15].…”