A common denominator of metabolic diseases, including type 2 diabetes Mellitus, dyslipidemia, and atherosclerosis, are elevated oxidative stress and chronic inflammation. These complex, multi-factorial diseases are caused by the detrimental interaction between the individual genetic background and multiple environmental stimuli. The cells, including the endothelial ones, acquire a preactivated phenotype and metabolic memory, exhibiting increased oxidative stress, inflammatory gene expression, endothelial vascular activation, and prothrombotic events, leading to vascular complications. There are different pathways involved in the pathogenesis of metabolic diseases, and increased knowledge suggests a role of the activation of the NF-kB pathway and NLRP3 inflammasome as key mediators of metabolic inflammation. Epigenetic-wide associated studies provide new insight into the role of microRNAs in the phenomenon of metabolic memory and the development consequences of vessel damage. In this review, we will focus on the microRNAs related to the control of anti-oxidative enzymes, as well as microRNAs related to the control of mitochondrial functions and inflammation. The objective is the search for new therapeutic targets to improve the functioning of mitochondria and reduce oxidative stress and inflammation, despite the acquired metabolic memory.

This article presents information on diabetes mellitus and its complications and its relationship with the mechanism of endothelial dysfunction based on previous studies. Type 2 diabetes is a chronic disease that significantly increases the risk of cardiovascular complications. Endothelial dysfunction is considered an early indicator of the diagnosis of diabetic vascular complications. Although the exact pathogenetic mechanisms of ED in diabetes mellitus are still unclear, at the initial stage it turned out that they trigger the synthesis of nitric oxide, oxidative phosphorylation of mitochondria, and other processes. The subsequent main factors influencing the activation of this process are dyspledemia, oxidative processes, and inflammation. The paper considers current literature data on hyperglycemia, oxidative stress, and glycation end products with endothelial changes. A separate section is devoted to oxidative stress and their significance in the development of endothelial dysfunction in diabetes mellitus. In addition, in this review, special attention is paid to the main mechanisms involved in the occurrence of endothelial dysfunction, the production of large amounts of reactive oxygen species (ROS), inflammation, as well as their relationship with the main factors of cardiovascular risk.