Today, stroke is the third most common pathology after cardiovascular disease and cancer, as well as the leading cause of disability in the world. Although some progress has been made in the field of primary and secondary stroke prevention over the past few decades, a deeper knowledge of the pathophysiology of the disease is needed to significantly improve diagnosis and therapy. MicroRNA (miRNA) is an important, recently identified class of posttranscriptional regulators of gene expression. MiRNA can be used as a tool for therapeutic interventions. This review considers a role of miRNAs in the regulation of experimental stroke and in the development of carotid artery stroke. A potential role of miRNAs as promising biomarkers of stroke is discussed.
In recent years, one of the promising areas in clinical medicine is the study of impaired ments in endothelial function and arterial wall stiffness, which can be referred to as one of the important predictors of cardiovascular events in patients with chronic kidney disease, including that of diabetic etiology. There is strong evidence that endothelial function and great artery stiffness may be used as reliable clinical and instrumental indicators to evaluate the efficiency of therapeutic measures and the rate of progression of cardiovascular disorders in type 2 diabetes mellitus. The article presents data on the role of endothelial dysfunction and arterial wall stiffness in the progression of chronic kidney disease in type 2 diabetes mellitus and discusses the possibility of their correction with pharmacological agents.
Infectious disease COVID-19 caused by the SARS-CoV-2 coronavirus is characterized by high contagiousness, complexity of pathogenesis and unpredictability of the clinical course. In severe cases, which are especially susceptible to men, the elderly and people with underlying medical conditions such as obesity, diabetes, hypertension, cardiovascular and chronic respiratory diseases, the infection leads to respiratory failure and death due to the development of an extensive inflammatory reaction. As a result of many studies, it has been established that one of the leading causes of the severe course and death of patients with COVID-19 is the development of coagulopathy, that is, increased thrombus formation in small vessels due to excessive activity of neutrophils, which form the so-called neutrophil extracellular traps (NETs). Although NETs play a useful role in protecting their host from pathogens, their overgrowth can trigger a cascade of adverse reactions including: the production of antibodies against the host’s DNA (autoimmunization); damage to surrounding tissue; or the occurrence of thromboembolic complications. Therefore, extracellular neutrophil traps and their markers have been identified as targets for new therapeutic strategies aimed at reducing the severity of COVID-19 disease and/or mortality. This article describes the structure of NETs, as well as analyzes the molecular mechanisms that contribute to their overgeneration. In addition, the prospects for COVID-19 therapy aimed at regulating the formation of extracellular traps by creating drugs both limiting the production of NET structures and dissolving their excess amounts in the body of patients are discussed.
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