Abstract:
The article analyzes literature data on the pathogenetic role of endothelial dysfunction, insulin resistance in the development of complications of metabolic dysfunction associated steatotic liver disease (MASLD), which has been considered by many to be a liver manifestation of metabolic syndrome for many years. Currently, two hypotheses of endotheliopathy development in MASLD are actively discussed. Supporters of the first hypothesis argue that endothelial dysfunction is derivative, that is, secondary to existing insulin resistance. The other hypothesis considers endothelial dysfunction as the cause of insulin resistance and concomitant conditions (hyperglycemia, hypertension, dyslipidemia). Atherosclerotic cardiovascular disease has long been recognized as an inflammatory disease, and the therapeutic benefit of anti-inflammatory drugs in the prevention of cardiovascular diseases has recently been demonstrated. The role of insulin resistance and concomitant hyperinsulinemia consists in direct and indirect atherogenic ef vascular walls. This pathophysiological process is the basis for the development of atherogenic dyslipidemia, a number of hormone secretion disorders and metabolic disorders. Over time, vascular wall remodeling occurs due to thickening of the arterial wall, which leads to an increase in total peripheral vascular resistance with normal smooth muscle tone. The cause is frequent vasoconstrictor effects, in which case the wall of the resistive vessels thickens, which limits local perfusion. The article discusses the pathogenetic mechanisms of the effect of hydrogen sulfide and nitric oxide molecules on the development of complications in MASLD, the role of physical exercise to correct some pathological conditions, and the role of the sympathoadrenal system.
